Some of the suitable examples of environmental hazards are:- 1. Electromagnetic Radiation 2. Arsenic 3. Chromium 4. Silica 5. Asbestos 6. Pesticides.
Example 1 # Environmental Hazards of Electromagnetic Radiation:
We are under continual attack from electromagnetic fields (EMFs) radiating from power lines, household wiring, microwave ovens, computers, televisions, clock radios, cellular phones, electric blankets, and other appliances. Researchers have correlated electro-pollution with increase in cancer, birth defects, depression, learning disabilities, chronic fatigue syndrome, Alzheimer’s disease, and sudden infant death syndrome.
Interaction between electricity and magnetic fields produces electromagnetic radiation. Electromagnetic radiation (EMR) r electromagnetic fields (EMFs) are the terms that broadly describe exposures created by the vast array of wired and wireless technologies that have altered our lives in beneficial ways. Though these technologies were designed to maximize energy efficiency and convenience; there is growing evidence about possible health risks associated with these technologies based on new studies. This is also called EMR hazards or RADHAZ.
EMF radiation passes through space at the speed of light at about 300 × 106 meters per second. We cannot see it, taste it or smell it, but it is one of the most pervasive environmental exposures in industrialized countries today. Human beings are bioelectrical systems. Our hearts and brains are regulated by internal bioelectrical signals. Environmental exposures to artificial EMFs can interact with fundamental biological process in the human body. In some cases, this can cause discomfort and disease.
EMFs are not blocked or weakened by the trees, walls, buildings, or other structures. Like X-ray, they pass through these objects and into our bodies- disrupting normal cellular function and biological processes.
Sources of Exposure to Electromagnetic Radiation:
Environmental and Natural:
Our greatest exposure to EMFs comes from within our homes and offices. All household and office appliances emit EMFs. But we cannot tell which are most dangerous by their size or function. Often the small devices like electric can openers and hair dryers are much more dangerous than the larger ones such as electric ovens or refrigerators.
The existence of non-thermal effects of EMFs on living matter, occur at every level from molecular to epidemiological.
Environmental exposure to man-made electromagnetic fields has been steadily increasing as growing electricity demand and ever-advancing technologies. Everyone is exposed to a complex mix of weak electric and magnetic fields, both at home and at work, from the generation and transmission of electricity, domestic appliances and industrial and industrial equipment, to telecommunications and broadcasting.
We are fundamentally electro-magnetic beings with micro electrical currents being generated to control our bodily functions such as growth, metabolism, thought, movements, etc. Disturbances to his electrical network in our body can cause malfunctioning of our internal organs, especially to the brain. Exposure to consistent external frequency for more than a few minutes can cause our body’s electrical functionality to be disrupted. This is true even with exposures to very weak EMFs.
At work, there are similar dangers- radiation sources and radiation enhancers. Certain occupations present more of a risk than others.
The workers listed below have the greatest radiation exposure daily:
Office workers are not safe either. They have to contend with fluorescent lighting, computers and other electronic devices that people rarely, hesitate to use.
According to their frequency and energy, electromagnetic waves can be classified as either ionizing radiations or non-ionizing radiations (NIR).
(i) Ionizing Radiations:
There are extremely high frequency electromagnetic waves (X-ray and gamma rays), which have enough photon energy to produce ionization by breaking the atomic bonds that hold molecules in cells together.
(ii) Non-Ionizing Radiations (NIR):
It is a term for that part of the electromagnetic spectrum which has photon energies too weak to break atomic bonds. They include ultraviolet radiation, infrared radiation, infrared radiation, radiofrequency and microwave fields. NIR cannot cause ionization however they have been shown to produce other biological effects, for instance by heating, altering chemical reactions or inducing electrical currents in tissues and cells.
There are four subgroups of electromagnetic radiation fields with frequency and intensity. This electromagnetic spectrum begins at a frequency of 1 Hertz (Hz), which is 1 wave/sec.
Hazards of EMFs:
An electromagnetic radiation hazard exists when electronic equipment generates a strong enough electromagnetic field to fall in a category listed below:
(i) Causes harmful or injurious effects to humans and wildlife.
(ii) Induces or otherwise couples currents and/or voltages of magnitudes large enough to initiate electro- explosive devices or other sensitive explosive components of weapons systems, ordnance, or other explosive devices.
(iii) Creates sparks large enough to ignite flammable mixtures or materials that must be handled in the affected areas. Electromagnetic fields above certain levels can trigger biological effects.
(iv) Short-term exposure at the levels present in the environment or in the home does not cause any apparent detrimental effects.
The EMF are not in themselves dangerous, they are not devastating our body cells like X-Rays, but our immune system is recognizing them as an enemy like a virus or bacteria. Fighting with them surrounding us everywhere makes our immune systems overtired which are not able to handle all tasks and are unable to completely defend our bodies e.g. catching cancer cells.
Even though RF/microwaves don’t have the energy to directly break chemical bonds, unlike ionizing radiation such as X-ray, there is scientific evidence that this energy can cause DNA damage indirectly leading to cancer by a combination of biological effects.
Radiation can damage the DNA in the cells of living things. Damaged DNA can make the cell stop working or unable to reproduce. It can also cause the cell to grow out of control, causing cancer.
Human bodies are very sensitive to EMFs. When we interact with natural energies, we reinforce the natural balance within our energy system. But when we are exposed to man-made EMFs that are unnatural for our bodies, they create a chaotic, situation that is harmful. Our bodies absorb and store the energy fields that weaken our immune system, resulting to various illnesses and diseases.
Some diseases linked to constant exposure to EMFs are- Headaches, disturbance in sleep patterns, shortened attention span, increased blood pressure, damage to eyes especially when glaucoma medication are also taken chronic fatigue syndrome, memory loss, miscarriages, birth defects, leukemia, lymphoma, brain tumor and even cancer.
1. Studies have shown EMF exposure above 2 mG will start to develop biological stress.
2. Evidence links prolonged exposure to levels between 2 and 12 mG+ with cancer and possible immune system effects.
3. Exposure to 12 mG suppresses the human hormone melatonin (critical for sleep, mood regulation, and overall health), powerful artificial EMFs overwhelm body’s electrical fields, changing their frequency and distorting the balance of the body’s electromagnetic field and its communication systems. This causes physical, mental and emotional chaos.
The danger doesn’t always pass once you get away from the strong electromagnetic field. That’s because biological systems have been proven to store electromagnetic radiation within the cells in the form of electromagnetic oscillations. These oscillations can stubbornly remain inside you, wreaking havoc with your body’s most important processes.
Environmental heat in excess of the mammalian thermoregulatory capacity can increase the permeability of the BBB to macromolecules. Neuronal albumin uptake in various brain regions was shown to be dose dependently related to brain temperature, with effects becoming apparent with temperature increases of 1°C or more. Thus, albumin bounded drugs uptake increases.
Despite regulatory protection against thermal effects, a small percentage of people have reported health problems that are believed to be caused by exposure to electromagnetic fields (EMF); for example from cell phone towers, Wi-Fi and cordless phones Authorities have labeled this group of people as having “electromagnetic hypersensitivity” or EHS. Common symptoms reported by people with EHS include heart palpitations, dizziness, nausea, digestive disturbances, fatigue, tiredness, difficulty concentrating, and skin irritation.
1 mG (milliGauss) is the common unit of measurement for magnetic fields. One milliGauss is 1/1000 of a Gauss. These fields are measured using an instrument called a milliGauss meter or Electrosmog Detector.
Today’s public exposure limits for telecommunications are based on the presumption that heating of tissue (for RF) or induced electric currents in the body (for ELF) are the only concerns when living organisms are exposed to RF. These exposures can create tissue heating that is well known to be harmful in even very short-term doses.
Bio-effects and some adverse health effects occur at far lower levels or RF and ELF exposure where no heating (or induced currents) occurs at all; some effects are shown to occur at several hundred thousand times below the existing public safety limits where heating is an impossibility.
For safety, the EPA recommends to limit magnetic field exposure to 0.5-5mG.
1. Keep your distance! EMFs are strongest at 0.5-1 meter or closer. Standing back from an appliance when it is in use as magnetic fields from appliances drop off dramatically in strength with increasing distance from the source. Don’t sit close to the back or sides of the monitor even when it is in another room or behind a partition.
2. Avoid unnecessary proximity to high EMF sources such as appliances including electric blankets and hair blow dryers.
3. Remove all electrical appliances at least 2metres way from bed.
4. Do not put cell phone under pillow as an alarm clock. It emits EMF even when not in use.
5. Reduce time spent in the field. Use electrical items for only brief periods. Switch off the power when not in use.
6. Correcting the household-wiring problem. Check the background field in home.
7. Purchase new appliances. The older the appliances, the greater the risk, as more EMFs are emitted.
8. Limit the time spent around home’s electrical appliances.
9. Place all clocks, cell phones, cordless phones and other electrical devices at least 2 meters from the place of sleep.
10. If one wears glasses, go for plastic frames or non-metal frames. Good conductor material can serve as an antenna to channel radio waves directly into brain.
11. Grow some plants indoors. Plants are natural eco-friendly air purifiers and their leaves can help absorb some infrared radiation and produce negative ions that are necessary for bodies.
12. Avoid prolonged exposure of children to television and computers.
The effects of EMFs on the health of individuals and environments are of concern to people.
Those who want to do something may consider the following suggestions:
1. Use for all members of family the Peace Ball, a personal device. Be sure, to wear it 24 hours every day.
2. Install a Neutralizer in house, car and in workplace.
WHO’s International EMF Project was launched to provide scientifically sound and objective answer to public concerns about possible hazards of low level electromagnetic fields.
Knowing that there is danger inherent in owning and operating cellular devices has not curbed the manufacture or selling strategies of cellular providers. This knowledge has not encouraged the government to stop cellular providers from raising the acceptable emissions allowances. This information hasn’t even inspired a cellular provider to voluntarily include a frequency-absorbing chip to protect their customers.
Cellular towers continue to be erected on office buildings sides and tops. Only monetary consideration between the building’s owners and the cellular providers determines the feasibility. The towers harm people by emitting very high levels of the RF radiation sometimes exceeding the guidelines. The harm is done to anyone in close proximity to the tower and certainly to the workers in the facility.
The warning symbol for radio frequency radiation hazards shall consist of a red isosceles triangle above an inverted black isosceles triangle, separated and outlined by an aluminum color border. The words “Warning- Radio-Frequency Radiation Hazard” shall appear in the upper triangle.
1. Low dose exposure doesn’t mean low risk. In fact, low-level EMF exposures increase health risks.
2. Everything generates an EMF. The natural earth creates one, and so does the human body. Human body creates an EMF of about 10 Hz.
3. There is no evidence to conclude that exposure to low level EMFs is harmful to human health.
4. Scientists say that chances of developing Alzheimer’s, Multiple sclerosis and Parkinson’s is enhanced by two minutes of exposure to emissions from mobile phones which can disable a safety barrier in blood causing proteins and toxins to leak into the brain.
5. The eyes and testes are the most vulnerable body organs to EMR.
Example 2 # Environmental Hazards of Arsenic:
Arsenic a metalloid element is a natural part of the earth’s crust in some part of the world and is found in water that has flowed through arsenic rich rocks. Arsenic is also emitted into air by burning of coal & vegetation and volcanic eruptions. High concentration of arsenic is found in drinking water in various parts of the world including India (in West Bengal).
Concentrations of arsenic in open ocean water are typically 12 μg/litre. The concentrations of arsenic in unpolluted surface water and groundwater are typically in the range of 110 μg/litre. Elevated concentrations in surface water and groundwater up to 100-5000 μg/litre can be found in areas of sulfide, mineralization.
Elevated concentrations (> 1 mg As/litre) in groundwater of geochemical origins have also been found in Taiwan, India (West Bengal) and more recently in most districts of Bangladesh.
Elevated arsenic concentrations were also found in the drinking-water in Chile, North Mexico and several areas of Argentina. Arsenic-contaminated groundwater was found in parts of PR China and the USA (California, Utah, Nevada, Washington and Alaska). More recently, arsenic concentrations of < 0.98 mg/litre have been found in wells in south-western Finland. Levels as high 35 mg As/litre and 25.7 mg As/litre have been reported in areas associated with hydrothermal activity.
Arsenic is the main constituent of more than 200 mineral species of which about 60% are arsenate, 20% sulfide and sulfosalts and the remaining 20% include, arsenides, arsenites, oxides & elemental arsenic.
Smelting of non-ferrous metals and the production of energy from fossil fuels are the two major industrial processes for anthropogenic arsenic contamination of air water and soil other sources of contamination are the manufacture and use of arsenical pesticides and wood preservatives.
Tailings from metal-mining operations are a significant source of contamination, and can lead to contamination of the surrounding topsails, and. because of leaching, sometimes the groundwater too could be contaminated As sulfur is often present in these tailings, exposure to the atmosphere in the presence of water leads to the production of an acid solution that cart teach many elements including arsenic.
Arsenic is also present in the rock phosphate used to manufacture fertilizers and detergents.
Past Agricultural Use:
In 1983, arsenical pesticides were one of the largest classes of bio-control agent. From the 1960s there was a shift in herbicide use, from inorganic compounds (including lead calcium arsenate and copper acetoarsenite) to inorganic and organic compounds (arsenic acid and sodium arsenate).
The levels of arsenic sewage sulfate reflect the extent of industrialization of the area served by the local sewage system. Significant quantities may be a mod by arsenic contaminated wastewater runoff derived from sources including atmospherically deposited arsenic residues from pesticide usage, phosphate detergents and. industrial effluent, particularly from the metal-processing industry.
There is the potential for significant occupational exposure to arsenic in several industries, e.g. non-ferrous smelting, electronics, wood preservation, wood joinery shops, arsenic production, glass manufacturing, and the production and application of arsenical pesticides. Exposure primarily through inhalation of arsenic- containing particulate, but ingestion and dermal exposure may be significant in particular situations e.g. preparation of CCA-treated timber.
It is extremely rare for workers to be exposed to arsenic alone the exposure is usually to arsenic in combination with other element.
Arsenic (a naturally occurring element) is a notoriously poisonous metalloid that has many allotropic forms; yellow, black and grey are a few that are regularly seen. Pure arsenic is a gray metal-like material usually found combined with other elements such as oxygen, chlorine, and sulphur.
Arsenic and its compounds are used as pesticides, herbicides, insecticides and various alloys. Arsenic in animals and plants combines with carbon and hydrogen to form organic arsenic compounds. Most inorganic and organic arsenic compounds are white or colorless powders that do not evaporate.
They have no smell, and most have no special taste. Most arsenic compounds can also dissolve in water. Arsenic cannot be destroyed in the environment. It can only change its form. Arsenic in air will settle to the ground or is washed out of the air by rain. Many arsenic compounds can dissolve in water.
Lead hydrogen arsenate has been used, well into the 20th century, as an insecticide on fruit trees (resulting in neurological damage to those working the sprayers), and in the 19th century as a coloring agent in sweets. Inorganic arsenic occurs naturally in many kinds of rock, especially in ores that contain copper or lead.
When these ores are heated at smelters to get the copper or lead, most of the arsenic enters the air as a fine dust. Smelters collect this dust and purify the arsenic for several uses. But once in the air, the arsenic particles travel with the wind for a while and then settle back to the ground.
Thus, arsenic can get into lakes, rivers, or underground water by dissolving in rain or snow, or through the discharge of industrial wastes. Some of the arsenic will stick to the sediment on the bottom of the lake or river, and some will be carried along by the water. The main use is as a preservative for wood to make it resistant to rotting and decay.
Inorganic arsenic compounds are also used to make several types of insect killers and weed killers are mainly used to preserve wood. Organic arsenic compounds are used as pesticides, primarily on cotton plants. Fish and shellfish can accumulate arsenic, but the arsenic in fish is mostly in a form that is not harmful.
Eating food, drinking water, or breathing air containing arsenic, working in Arsenic using industries, smoke from wood treated with arsenic, living near uncontrolled hazardous waste sites containing arsenic, living in areas with unusually high natural levels of arsenic in rock are a few important sources of the metal. In the past, several kinds of products used in the home (rat poison, ant poison, weed killer, some types of medicines) had arsenic in them.
Health effects of inorganic arsenic are sore throat or irritated lungs, nausea, vomiting, decreased production of red and – white blood cells, abnormal heart rhythm, damage to blood vessels, a sensation of “pins and needles” in hands and feet, redness and swelling of the skin and even death, central and peripheral nervous system disorders are a common occurring amongst workers in Arsenic rich environment.
Long term exposure to inorganic arsenic are peripheral neuropathy, darkening of the skin and the appearance of small “corns” or “warts” on the palms, soles, and torso and liver or kidney damage in humans. Inorganic arsenic can increase the risk of lung cancer, skin cancer, bladder cancer, liver cancer, kidney cancer, and prostate cancer. Organic arsenic compounds are less toxic than inorganic arsenic compounds. Arsenic and many of its compounds are especially potent poisons.
Arsenic kills by inhibition of the metabolic enzyme lipothiamide pyrophosphatase, leading to death from multi-system organ failure. The IARC recognizes arsenic and arsenic compounds as group 1 charcinogens, and the EU lists arsenic trioxide, arsenic pentoxide and arsenate salts as category 1 carcinogens. Chronic arsenic poisoning from drinking water causes a disease known as Arsenicosis.
Non-occupational human exposure to arsenic in the environment is primarily through the food and water. Of these, food is generally the principal contributor to the daily intake of total arsenic. In some areas, arsenic in drinking-water often constitutes the principal contributor to the daily arsenic intake.
Contaminated soils such as mine tailings are also a potential source of arsenic exposure. The daily intake of total arsenic from food and beverages is generally between 20 and 300 μg/day. Approximately 25% of the arsenic present in food is inorganic, but this depends highly on the type of food ingested inorganic arsenic levels in fish and shellfish are low (< 1%). Foodstuffs such as meat, poultry, dairy products and cereals have higher levels if inorganic arsenic.
Pulmonary exposure may contribute up to approximately 10 μg day in a smoker and about 1 μg/day in a non-smoker and more in polluted areas. The concentration of metabolites of inorganic arsenic in urine (inorganic arsenic) reflects the absorbed dose of inorganic arsenic by an individual. Generally, it ranges from 5 to 20 μg As/litre, but may even exceed 1000 μg litre.
Because arsenic is a recognized carcinogen, focus has been on cancer risks. Studies have also examined effects of arsenic on atherosclerotic diseases diabetes mellitus and peripheral vascular diseases in different geographical areas and under varying exposure conditions following are the principal health effects of arsenic exposure-
Inorganic arsenic is acutely toxic and ingestion of large doses leads to gastrointestinal symptoms, disturbances of cardiovascular and eventually nervous system functions, multiorgan failure and eventually death. In survivors, tone marrow depression, haemolysis, hepatomegaly, melanosis, polyneuropathy and encephalopathy may be observed.
Vascular effects include heart disease and high blood pressure, which are caused by a progressive narrowing of blood vessels that diminishes me normal flow of blood. The flow through small vessels in the extremities ran be reduced so severely that tissue starves and dies.
Untreated can lead to gangrene of the feet or black foot disease, a condition seen in people from Bangladesh and other regions of the world where arsenic concentration in drinking water die above 500parts per billion (500 micrograms per liter). In contrast, people drinking water with less than 500 parts per billion may be at a greater risk for hypertension and heart attacks.
Non-occupational exposure occurs mainly through drinking water. Exposure to levels of arsenic in drinking water well above 100 ppb has been associated with an increased risk of type 2 diabetes in the high- arsenic areas Taiwan and Bangladesh. The biological mechanisms for an association between chronic arsenic exposure and increased diabetes risk are not known.
Human exposure to arsenic causes nervous system disturbances such as polyneuropathy, EEG abnormalities and in extreme cases, hallucination, disorientation and agitation.
Skin changes, including hyperpigmentation and generalized hyperkeratosis, are the most common signs of chronic at ingestion from drinking water.
Arsenic Rule at a Glance:
(i) Maximum Contaminant Level (MCL) – MCL-0.010 ppm
(ii) Maximum Contaminant Level ground (MCLG) – MCLG-0.005 ppm
Skin damage or problems with circulatory systems, and may haw increased risk of getting cancer.
Sources of Contamination:
Erosion of natural deposits runs off from orchards, run off from glass and electronic production wastes.
Ingestion of arsenic is known to cause skin cancer. The evidence indicates that arsenic can also cause liver, lung, kidney and skin cancer.
Occupation exposure to arsenic, primary by inhalation, is associated with lung cancer. Increased risks have been observed at cumulative exposure levels > 0.75(mg/m3)/year (e.g. 15 year exposure to a work room air concentration 50 μg/m3).
Smokers are exposed to arsenic by the inhalation of mainstream cigarette smoke. It has been estimated that someone smoking 40 cigarettes per day would inhale about 10 jag of arsenic.
Biomarkers of Arsenic Exposure:
Inorganic arsenic is rapidly cleared from blood; hence blood arsenic is typically used only as an indicator of very recent or relatively high-level exposure. (E.g. in cases of poisoning), or chronic stable exposure (e.g. to drinking water). The limitation of blood arsenic levels as indicators of low-level exposure of drinking water is that it is difficult to distinguish the contributions of inorganic arsenic from water and organic arsenic from food.
Hair and Nail:
As arsenic accumulates in keratin-rich tissues such as skin, hair and nail as a consequence of its affinity for sulfhydryl groups, arsenic levels in hair and nails may be used as an indicator of past arsenic exposure. When exposed to water containing high arsenic levels, hair can bind arsenic extremely and may not be removed readily by washing.
The arsenic content of fingernails and toenails has also been used as bio-indicators of past arsenic exposure and fingernail arsenic has been reported to be significantly correlated with hair arsenic content.
Since arsenic is rapidly metabolized and excreted through the urine, total arsenic, inorganic arsenic and the sum of arsenic metabolites in urine have all been used as biomarkers of recent arsenic exposure. Levels of arsenicals in urine may be a consequence of inhalation exposure or ingestion of arsenic from drinking water, beverages, soil or foodstuffs.
Purification of Water:
Arsenic Removal Units (ARUs):
The arsenic removal units are designed to both remove arsenic from the ground-water making it safe for human consumption and provide for safe containment of the removed arsenic without long-term adverse ecological impact.
The ARU lowers the arsenic concentration from as high as 500 parts per billion to less than 50 parts per billion more than 150, 000 villagers in Bangladesh and West Bengal are drinking and using arsenic safe potable water from ARUs attached to ground well pumps which do not require chemical additions, pH adjustments or electricity, Water is pumped from the well prior to installation of the well-head unit where it passes through beads of activated alumina that remove the arsenic.
Only indigenous durable materials are used in constructing the ARUs Many such units have been providing safe water for well over five years.
To combat the arsenic crisis following steps should be taken:
1. In most of the villages surveyed in West Bengal and Bangladesh, an average of 35% of the tube wells contains water that is safe to drink. The mouths of the safe tube wells must be colored green and the unsafe ones red so that the villagers can use water from green tube wells for drinking and cooking, and red tube wells water for bathing washing toiled, etc. The safe tube wells should be tested for arsenic every 3-6 months.
Arsenic Fact Sheet:
1. Arsenic is naturally present at high levels in the groundwater of a number of countries.
2. Arsenic is highly toxic in its inorganic form.
3. Contaminated water used for drinking, food preparation and irrigation of food crops poses the greatest threat to public health from arsenic.
4. Long-term exposure to arsenic from drinking-water and food can cause cancer, skin lesions developmental effects, cardiovascular disease, neurotoxicity and diabetes.
5. The most important action in affected communities is the prevention of further exposure to arsenic by provision of a safe water supply.
Sources of Arsenic Exposure:
Arsenic is a natural component of the earth’s crust and is widely distributed throughout the environment in the air, water and land. It is highly toxic in its inorganic form.
People are exposed to elevated levels of inorganic arsenic through drinking contaminated water, using contaminated water in food preparation and irrigation of food crops, industrial processes, eating contaminated food and smoking tobacco.
Long-term exposure to inorganic arsenic, mainly through drinking of contaminated water, eating of food prepared with this water and eating food irrigated with arsenic- rich water, can lead to chronic arsenic poisoning. Skin lesions and skin cancer are the most characteristic effects.
The greatest threat to public health from arsenic originates from contaminated groundwater. Inorganic arsenic is naturally present at high levels in the groundwater of a number of countries, including Argentina, Bangladesh, Chile, China, India, Mexico, and the United States of America. Drinking-water, crops irrigated with contaminated water and food prepared with contaminated water are the sources of exposure.
Fish, shellfish, meat, poultry, daily products and cereals can also be dietary sources of arsenic, although exposure from these foods is generally much lower compared to exposure through contaminated groundwater. In seafood, arsenic is mainly found in its less toxic organic form.
Arsenic is used industrially as an alloying agent, as well as in the processing of glass, pigments, textiles, paper, metal adhesives, wood preservatives and ammunition. Arsenic is also used in the hide tanning process and, to a limited extent, in pesticides, food additives and pharmaceuticals.
People who smoke tobacco can also be exposed to the natural inorganic arsenic content of tobacco because tobacco plants essentially take up arsenic naturally present in the soil. Also, in the past, the potential for elevated arsenic exposure was much greater when tobacco plants used to be treated with lead arsenate insecticide.
Arsenic occurs in inorganic and organic forms. Inorganic arsenic compounds (such as those found in water) are highly toxic while organic arsenic compounds (such as those found in seafood) are less harmful to health.
The immediate symptoms of acute arsenic poisoning include vomiting, abdominal pain and diarrhoea. These are followed by numbness and tingling of the extremities, muscle cramping and death, in extreme cases.
The first symptoms of long-term exposure to high levels of inorganic arsenic (e.g. through drinking-water and food) are usually observed in the skin, and include pigmentation changes, skin lesions and hard patches on the palms and soles of the feet (hyperkeratosis). These occur after a minimum exposure of approximately five years and may be a precursor to skin cancer.
In addition to skin cancer, long-term exposure to arsenic may also cause cancers of the bladder and lungs. The International Agency for Research on Cancer (IARC) has classified arsenic and arsenic compounds as carcinogenic to humans.
Other adverse health effects that may be associated with long-term ingestion of inorganic arsenic include developmental effects, neurotoxicity, diabetes and cardiovascular disease. In China (Province of Taiwan), arsenic exposure has been linked to “black-foot disease”, which is a severe disease of blood vessels leading to gangrene. However, this disease has not been observed in other parts of the world, and it is possible that malnutrition contributes to its development.
Arsenic contamination of groundwater is widespread and there are a number of regions where arsenic contamination of drinking-water is significant.
Arsenic in Bangladesh has attracted much attention since recognition in the 1990s of its wide occurrence in well-water in that country. People in Bangladesh are at risk of being exposed to arsenic concentrations that are greater than the national standard of 50 microgram/litre and the WHO guideline value of 10 μg/litre respectively.
The symptoms and signs caused by long-term elevated exposure to inorganic arsenic differ between individuals, population groups and geographical areas.
There is no method to distinguish cases of cancer caused by arsenic from cancers induced by other factors.
Prevention and Control of Arsenic Poisoning:
There are a number of options as discussed below to reduce levels of arsenic in drinking-water, food preparation water and water used for irrigation of food crops.
(i) Substitute high-arsenic sources such as groundwater, with low-arsenic, microbiologically safe sources such as rain water and treated surface water. Low- arsenic water can be used for drinking, cooking and irrigation purposes, whereas arsenic-rich water can be used for other purposes such as bathing and washing clothes.
(ii) Discriminate between high-arsenic and low-arsenic sources. For example, test water for arsenic levels and paint tube wells or hand pumps in different colours. This can be an effective and low-cost means to rapidly reduce exposure to arsenic.
(iii) Blend low-arsenic water with higher-arsenic water to achieve an acceptable arsenic concentration level.
(iv) Install arsenic removal systems – either centralized or domestic – and ensure the appropriate disposal of the removed arsenic. Technologies for arsenic removal include oxidation, coagulation- precipitation, absorption, ion exchange and membrane techniques. There are an increasing number of effective and low-cost options for removing arsenic from small or household supplies.
Long-term actions are also required to reduce occupational exposure from industrial processes.
High-risk populations should also be monitored for early signs of arsenic poisoning usually skin problems.
Arsenic is one of WHO’s 10 chemicals of major public health concern. The current recommended limit of arsenic in drinking-water is 10 μg/liter, although this guideline value is designated as provisional because of measurement difficulties and the practical difficulties in removing arsenic from drinking-water.
Example 3 # Environmental Hazards of Chromium:
Chromium (Cr) is a lustrous, brittle, hard metal having silver-gray colour and can be highly polished. When heated it burns and forms the green chromic oxide. Chromium is unstable in oxygen, it immediately produces a thin oxide layer that is impermeable to oxygen and protects the metal.
Chromium is naturally found in rocks, animals, plants, and soil. It can exist in several different forms. Depending on the form it takes, it can be a liquid, solid, or gas. The most common forms are chromium (O), chromium (III), and chromium (VI). No taste or odor is associated with chromium compounds.
Chromium (III) is an essential nutrient that can be toxic in large doses. The National Academy of Sciences (USA) has established a safe and adequate daily intake for Cr(III) in adults of 50 -200 micrograms per day. Major factors governing the toxicity of chromium compounds are oxidation state and solubility.
Since Cr(III) is poorly absorbed by any route, the toxicity of chromium is mainly attributable to the Cr(VI) form. It can be absorbed by the lung and gastrointestinal tract, and even to a certain extent by intact skin. Any of these species could attack DNA, proteins, and membrane lipids, thereby disrupting cellular integrity and functions.
Chromium is known to enhance the action of insulin, a hormone critical to the metabolism and storage of carbohydrate, fat, and protein in the body. Chromium also appears to be directly involved in carbohydrate, fat, and protein metabolism.
Occurrence of Chromium in Nature:
Sources of Chromium Exposure:
Occupational exposures to chromium occur to workers through:
1. Chromate added in anti-algae
2. Antifreeze agents
3. Cement, Chrome alloy production
4. Chrome electroplating (Cr[VI])
5. Copier servicing, Glassmaking
6. Leather tanning (soluble Cr[III])
7. Paints/pigments (insoluble Cr[VI])
8. Photoengraving, Porcelain and ceramics manufacturing
9. Production of high-fidelity magnetic audiotapes
10. Tattooing, Textile manufacturing
11. Welding of alloys or steel
12. Wood preservatives, i.e. acid copper chromate
Environmental exposures to chromium occur to workers through:
1. Air borne emissions from chemical plants and incineration facilities
2. Cement dust, contaminated landfill Effluents from chemical plants
3. Asbestos lining erosion
4. Road dust from catalytic converter erosion and asbestos brakes
5. Tobacco smoke
6. Top soil and rocks
Routes of Exposure:
Chromium exposure can occur by breathing in breathing in dust or by skin contact with solutions or solids or by eating, drinking or smoking in areas where chromium is used. Members of the public could be exposed to it due to a spillage or inadequate safety measures during disposal/incineration, most often by ingestion through chromium content in soil, food, and water.
Chromium enters the air, water and soil in the chromium (III) and chromium (VI) form through natural processes and human activities.
In India, about 20000-32000 tons of elemental Cr annually escapes into the environment from tanning industries. Even if the recommended limit for Cr concentration in water are set differently for Cr(III) (8 (μg/L) and Cr(VI) (1 μg/L), it ranges from 2 to 5g/L in the effluents of these industries.
Only 10% of Americans have an adequate amount of chromium in his/her diet.
There is no specific recommended daily allowance for chromium. Average daily intake may be about 80-100 mcg. Even mild deficiencies of chromium can produce problems in blood sugar metabolism, such as anxiety or fatigue. Abnormal cholesterol metabolism and increased progress of atherosclerosis are associated with chromium deficiency, and deficiency may also cause decreased growth in young people and slower healing time after injuries or surgery.
Irrespective of the route of exposure, the initial approach to an affected individual includes a brief assessment of clinical status followed by support of basic cardiopulmonary functions. Once the airway has been stabilized and cardiopulmonary support has been instituted as indicated, further measures can be considered.
Management of Acute Chromium Toxicity:
1. No proven antidote is available for chromium poisoning. Acute poisoning is often fatal regardless of therapy. Treatment in cases of acute high-level chromium exposure is usually supportive and symptomatic.
2. Fluid and electrolyte balance is critical.
3. Affected patients should be monitored carefully for evidence of gastrointestinal bleeding, hemolysis, coagulopathy, seizures and pulmonary dysfunction. Appropriate supportive measures may include ventilator support, cardiovascular support, and renal and hepatic function monitoring.
4. When renal function is compromised, maintenance of adequate urine flow is important. Progression to anuria is associated with poor prognosis.
5. Induction of vomiting is contraindicated, owing to the potential corrosive effects of the chromium compounds and the potential for rapid deterioration of the patient.
6. Gastric lavage with magnesium hydroxide or another antacid might be useful in cases of chromium ingestion.
7. If renal failure ensues, hemodialysis may be necessary for management of the renal failure itself.
8. If the eyes and skin are directly exposed, flush with copious amounts of water.
9. The ulcers heal in several weeks without specific treatment.
10. EDTA ointment 10% might facilitate removal of chromate scabs.
11. Weeping dermatitis can be treated with 1% aluminum acetate wet dressings, and chrome ulcers can be treated with topical ascorbic acid.
Management of Chronic Chromium Toxicity:
1. In most patients with chronic low-dose exposure, no specific treatment is needed.
2. The mainstay of management is removing the patient from further exposure and relying on the urinary and fecal clearance of the body burden.
3. Dermatitis, liver and renal injury will not progress after removal from exposure, and, in most cases, the patient will recover.
4. If the exposure has been to high levels or lengthy, the increased risk of lung cancer should be examined.
5. Although no reliable tests are currently available to screen patients for lung cancer, the physician can provide advice and patient education regarding smoking cessation, avoiding or minimizing exposure to other known pulmonary carcinogens, and general preventive health measures.
6. Annual chest radiographs advisable in selected cases.
Prevention of Chromium Toxicity:
1. Wear proper personal protective equipment such as respiratory protection, protective clothing eye protection, and gloves.
2. Maintain work area free of dust.
3. Shower and change clothes immediately on completion of work.
4. Leave or dispose of contaminated clothing at the worksite.
5. Do not track dust from the work area to the rest of the home.
6. Do not smoke, eat, or drink in the work area.
7. Wash hands well before eating, drinking, or smoking.
8. Head employer should provide patient and worker education.
9. If a smoker, stop smoking.
Avoid Tobacco Smoke:
Chromium is a component of tobacco smoke. Avoid smoking in enclosed spaces like inside the home or car in order to limit exposure to children and other family members.
Launder Clothing from Worksites:
Clothing or items removed from the workplace may contain chromium if employed in a setting where occupational exposure is significant. Therefore, common sense hygiene and laundry practices may help avoid unnecessary exposures.
Patients should be advised to call if they develop any of the following symptoms:
1. Symptoms of kidney dysfunction such as lower extremity swelling, reduced urine volume changes in color of urine, etc.
2. Dyspnea, cough, wheezing, nausea, vomiting, diarrhea
3. Yellowing of the teeth
4. Altered sense of smell
For in situ remediation of soil and groundwater, a variety of geochemical fixation or anaerobic biological treatment methods have been designed which make use of Cr’s ability to change the valence state of the oxidized, toxic and highly mobile nature of Cr(VI) and convert it into the more stable, nontoxic, and immobile Cr(III). Cr(III) ultimately precipitates out as Cr(III) hydroxide [Cr(OH)3]. In these technologies, Cr is generally not removed from the environment, but becomes less toxic and immobile.
Many treatment methods use sulfur-based reductants; anaerobic biodegradation enhancements such as lactic acids, molasses, or other chemical reductants; or elemental iron [Fe(O)] technologies to create a reducing environment.
A variety of technologies are used in the extraction and treatment of surface water or groundwater (known as pump and treat).
Once on the surface, water containing Cr(VI) can be reduced by Fe(II) compounds followed by several procedures including alkaline precipitation, ion exchange with regenerate treatment, or disposal.
Electrochemical reduction is another method used where Cr (VI) reduction is followed by alkaline precipitation in which Fe(III) forms electrochemically, instead of being added as a purchased chemical, and acidic reduction of the Cr at pH < 3.0 with sulfur dioxide, sodium sulfite, sodium bisulfite, or sodium meta bisulfite completes the conversion to Cr(III).
If reduction with a sulfite compound is used, there is a greater potential for incomplete conversion of Cr(VI) to Cr(III). Consequently, these reactions must be monitored carefully to ensure complete conversion to Cr(III), which ultimately precipitates out of solution as Cr(OH)3.
Example 4 # Environmental Hazards of Silica:
The chemical compound silicon dioxide, also known as silica or silox is the oxide of silicon (chemical formula SiO2) and has been known for its hardness. Silica is commonly found in nature as sand or quartz. It is a principal component of most types of glasses and some other substances such as concrete.
Free silica exists in two main forms- amorphous silica and crystalline silica. Crystalline silica is one of the most common minerals found on the surface of the earth. It may be found in a variety of forms the most common of which is quartz. Other types of crystalline silica include tridymite and cristobalite.
Amorphous silica is the term used to describe forms, which have no regular crystal structure. It includes a wide range of fossilized skeletal remains of marine organisms. While there is some scientific evidence that amorphous silica may occasionally cause adverse health effects, most silica-related disease has been a result of breathing of crystalline silica.
Chronic exposure to crystalline silica is associated with increased incidences of tuberculosis, bronchitis, emphysema, chronic obstructive pulmonary disease, renal diseases, silicosis and lung cancer. Of these potential health effects silicosis and lung cancer are the effects of most concern associated with occupational exposure to reparable quartz dust.
Crystalline silica in the form of quartz or cristobalite from occupational sources is (carcinogenic to humans. The severity and incidence of silicosis and silica induced cancer increases with intensity of dust exposure, with increased cumulative duration of exposure, with increasing peak concentrations of silica and with increased percentage of silica within the respirable dust.
Silicosis (Disease Caused by Silica):
Silicosis is the chronic fibrosing disease of the lungs produced by the prolonged and extensive exposure to free crystalline silica dust. When workers inhale crystalline silica (dust), the lung tissue reacts by developing fibrotic nodules and scarring around the trapped silica particles.
This fibrotic condition of the lung is called silicosis. If the nodules grow too large, breathing becomes difficult and death may result. Silicosis victims are also at high risk of developing active tuberculosis. Silicosis treatment is very limited as there is no cure for the disease, but it is 100 percent preventable if employers, workers, and health professionals work together to reduce exposure.
Types of Silicosis:
i. Chronic Silicosis:
Results from long-term exposure (more than 20 years) to low amounts of silica dust. Nodules of chronic inflammation and scarring provoked by the silica dust form in the lungs and chest lymph nodes. This disease may feature breathlessness and may resemble chronic obstructive pulmonary disease (COPD) Chronic silicosis can be simple silicosis or complicated silicosis (also called progressive massive fibrosis), a distinction based on the chest radiographic appearance.
Simple Silicosis may be asymptomatic or may present with exertional dyspnea and cough with sputum production.
Complicated Silicosis, dyspnea and productive cough often are accompanied by constitutional symptoms of malaise and weight loss.
ii. Accelerated Silicosis:
Occurs after exposure to larger amounts of silica over a shorter period of time (4-8 years). Inflammation, scarring, and symptoms progress faster in accelerated silicosis than in simple chronic silicosis.
iii. Acute Silicosis:
Results from short-term exposure to very large amounts of silica mainly in unregulated environments. The lungs become very inflamed and may fill with fluid, causing severe shortness of breath and low blood oxygen levels. Acute silicosis causes symptoms of severe dyspnea, cough, fever, and weight loss.
On chest radiograph, ground-glass appearances, as well as coarse linear or rounded opacities are seen. A miliary picture with very small round opacities may also occur in the lower lung fields. The diagnosis of alveolar proteinosis may be readily made by the appearance of the bronchoalveolar fluid, which has a milky appearance.
Particles of silica dust get trapped in the tiny sacs (alveoli) in the lungs where air exchange takes place. White blood cells called macrophages in the alveoli ingest the silica and die. The resulting inflammation attracts other macrophages to the region.
The nodule forms when the immune system forms fibrous tissue to seal off the reactive area. The disease process may stop at this point, or speed up and destroy large areas of the lung. The fibrosis may continue even after the worker is no longer exposed to silica.
Early symptoms of silicosis include shortness of breath after exercising and a harsh, dry cough. Patients may have more trouble in breathing and cough up blood as the disease progresses.
Congestive heart failure can give their nails a bluish tint. Patients with advanced silicosis may have trouble in sleeping and experience chest pain, hoarseness, and loss of appetite.
Other Silica Related Diseases:
i. Chronic Obstructive Pulmonary Disease (COPD):
Chronic obstructive Pulmonary Disease is a term used for a number of conditions, including chronic bronchitis and emphysema COPD leads to damaged airways in the lungs, causing them to become narrower and making it harder for air to get in and out of the lungs.
Exposure to silica and coal mine dusts may result in chronic obstructive pulmonary disease, including emphysema and chronic bronchitis that appears indistinguishable from obstructive lung disease caused by exposure to tobacco smoke. This may cause significant respiratory dysfunction in sensitive individuals.
ii. Pulmonary Tuberculosis:
Exposure to crystalline silica dust causes multiple diseases, but silicosis and silica dust-associated tuberculosis (TB), in particular, are the two diseases that remain high on the list of occupational health priorities. The prevalence of silica-related TB is exacerbated by the human immunodeficiency virus (HIV) epidemic in low- income countries.
The relative risk for tuberculosis is more for men with silicosis compared with that in the men without silicosis.
iii. Autoimmune Disorders:
There have been reports linking silica exposure to a variety of autoimmune diseases (systemic sclerosis, rheumatoid arthritis, lupus, chronic renal disease). Evidence of this association in larger epidemiologic studies has been increasing in the last decade.
iv. Renal Diseases:
Silica exposure has been associated with kidney disease (chronic renal disease and glomerulonephritis). Excess risk of end-stage renal disease due to a lifetime of occupational exposure at currently recommended limits is above a background end-stage renal disease risk.
Caplan’s syndrome is characterized by the presence of seropositive rheumatoid arthritis associated with a specific form of pneumoconiosis, consisting of multiple, well-defined homogeneous rounded opacities on chest X-ray. It develops especially in miners working in anthracite coal-mines and in persons exposed to silica and asbestos. In the development of the disease, genetic factors are considered to play an important role by influencing immunological reactivity of the organism exposed to various hetero-antigens.
Silica exposed men had increased risk of rheumatoid arthritis, with an odds ratio (OR), adjusted for age, residential area, and smoking.
Prevention and Control of Silica Related Diseases:
Employers and workers should take appropriate actions to reduce silica flour exposure to below permissible limits.
This can be accomplished by following measures:
Workers exposure surveys should be made by competent industrial hygienist and engineer. Surveys are necessary to determine the extent of worker exposure and the effectiveness of engineering controls. In the collected air samples, crystalline silica is measured by-
XRD (filter re-deposition) (X Ray Diffraction) FTIR (KBr pellet) Fourier Transform infrared spectrophotometry.
The most effective control of airborne concentrations of silica flour is at the source of contamination by enclosure of the operation and/or use of local exhaust ventilation.
Pre-placement and annual medical examinations should be made available to all workers who manufacture, use or handle silica flour or materials containing silica flour.
Workers with radiographic evidence of silicosis should be given the opportunity to get transferred to other jobs/department having no silica exposure (defined as exposure at concentrations less than half of the recommended standard).
The following work practices are recommended:
(a) Work procedures should be developed so they do not produce dust.
(b) Work clothes should be vacuumed before removal.
(c) General housekeeping duties should be intensified so that there is no dust accumulation on machinery, beams, corners, and other surfaces. Dustless methods of cleaning such as vacuuming or wetting down should be used. Dry sweeping or blowing with com pressed air should be avoided.
(d) Emphasis should also be given to cleanup of spills, preventive maintenance, and timely repair of equipment.
Personal protective equipment is not recommended as a primary means of control.
Exposure of workers to airborne silica flour should not be controlled with the use of respirators except:
(a) During installation and implementation of engineering or work practice controls;
(b) In work situations in which engineering and work practice controls are technically not feasible;
(c) During major overhaul and repair of equipment, if exposure to silica flour is possible;
(d) In operations that require entry into tanks or closed vessels; or
(e) In emergencies.
Worker education is a vital aspect of a good control program. Workers should be informed of the hazardous nature of silica flour, the results of workplace monitoring and medical tests, and the correct usage and maintenance of respirators.
7. Labeling of Silica Flour Containers:
Packaged silica flour should be labeled correctly, and health warnings should be placed on each container to alert users, handlers and producers to the hazards of silica flour.
i. Agate Grinding Units:
Local exhaust system containing air-cleaning device was developed and fitted over grinding machine along with bag fitter especially designed for agate grinding. The exhaust system did not interfere with the work and the workers found it very useful as it facilitated the work by removing the dust, which hampered their sight. To reduce electricity consumption, the emery wheel and blower were rotated with the same motor by attaching it to a pulley. Dust reduced by about 93% in the work environment.
ii. Silica Flourmills (Hammer-Mill):
The crushing process involves jaw crusher, disintegration, screening and bagging. Dust control device was developed with bag filter and installed. Since jaw crusher is outside the shed, separate dust control device was developed and installed with motors. Dust control measures like, enclosure of dust source, use of powerful exhaust and humidification of work environment, reduced dust by about 75-85%.
iii. Stone Quarry:
Developed a protective shield of dust hood made of an iron frame covered by an acrylic shield at its food and cloth on its sidewalls. The dust hood could be fitted to a chisel. The height of the hood could be adjusted. Workers satisfied with the device as it reduced the dust exposure.
iv. Silica Flourmill (Ball-Mill):
NIOH designed Dust control system using ACGIH ventilation guidelines which involves hood, ducting, centrifugal fan and bag filters with reverse pulse jet system. Owners were encouraged to install dust control system for feeding and bagging operations. The work is in progress for testing the efficacy of dust control system.
Example 5 # Environmental Hazards of Asbestos:
The name asbestos comes from the word asbestos, which in Greek meant unquenchable, inextinguishable, or indestructible. The Romans, called asbestos by the name of amiantus, used it in their building materials, cremation cloths, lamp wicks, and even made napkins.
Asbestos clothing was also used by the Egyptians to dress their pharaohs at the time of burial, by the ancient Finnish to strengthen pottery, and in the middle ages as insulation for armor.
New applications began to expand the usage of asbestos. It was used in steam locomotives to insulate their boilers, pipes, and fireboxes, as well as line their brakes and clutches; it was made into packing’s, gaskets and pipe lagging materials and was even used for protective suits by firemen.
In the 1900s the use of asbestos began to increase dramatically. Military began to make use of it in ships, flares, and fireproof suits among other things. Since reaching its peak in 1973 asbestos production and consumption has been on a constant decrease and many countries including Germany, Italy, Netherlands, Sweden, Norway, Denmark, and Switzerland have passed comprehensive bans on asbestos mining, production, sale, use, import and export.
Asbestos is not a single substance, but is the generic name for a family of six related polysilicate fibrous minerals of which one (chrysotile) belongs to the serpentine family and five (actinolite, amosite, anthophyllite, crocidolite, and tremolite) belong to the amphibole family.
These minerals differ from each other in physical and chemical properties, and each mineral can exist in a wide range of fiber sizes. These differences between fiber type and, more importantly, fiber size (length and diameter) are believed to be important determinants of the health risks posed by asbestos.
i. Mining Activities:
Exposure to asbestos can occur in workers involved in mining, milling and handing of other ores and rocks containing asbestos. Residents who live near mining, milling or manufacturing sites that involve asbestos- containing material may be exposed to higher levels of airborne asbestos.
ii. Demolition and Maintenance Work:
Amphibole asbestos can be found in a variety of building materials, such as insulation, ceiling or floor tiles, and cement pipes. Workers or homeowners involved in demolition work, maintenance, repair, or remodeling of buildings containing these products can be exposed to higher airborne levels than in ambient air.
Some of the work environments or occupations in which workers are exposed include:
1. When asbestos fibers are inhaled, most fibers are expelled, but some can become lodged in the lungs and remain there throughout life. Fibers can accumulate and cause scarring and inflammation. Enough scarring and inflammation can affect breathing, leading to disease.
2. The term “naturally occurring asbestos” refers to the mineral as a natural component of soils or rocks as opposed to asbestos in commercial products, mining or processing operations. Naturally occurring asbestos can be released from rocks or soils by routine human activities, such as construction, or natural weathering processes.
3. People are more likely to experience asbestos-related disorders when they are exposed to high concentrations of asbestos, are exposed for longer periods of time, and/or are exposed more often.
4. Exposure to asbestos can increase the likelihood of lung cancer, mesothelioma, and non-malignant lung conditions such as asbestosis (restricted use of the lungs due to retained asbestos fibers) and changes in the pleura (lining of the chest cavity, outside the lung).
5. Changes in pleura such as thickening, plaques, calcification, and fluid around the lungs (pleural effusion) may be early signs of asbestos exposure. These changes can affect breathing more than previously thought. Pleural effusion can be an early warning sign for mesothelioma (cancer of the lining of the lungs).
6. Most cases of asbestosis or lung cancer in workers occurred 15 years or more after the person was first exposed to asbestos.
7. Most cases of mesothelioma are diagnosed 30 years or more after the first exposure to asbestos.
8. Asbestos-related disease has been diagnosed in asbestos workers, family members, and residents who live close to asbestos mines or processing plants.
9. Health effects from asbestos exposure may continue to progress even after exposure is stopped.
1. Exposure concentration – what was the concentration of asbestos fibers?
2. Exposure duration – how long did the exposure time period last?
3. Exposure frequency – how often during that time period was the person exposed?
4. Size, shape and chemical makeup of asbestos fibers.
5. Individual risk factors, such as a person’s history of tobacco use (smoking) and other pre-existing lung disease, etc.
Cigarette smoke and asbestos together significantly increase chances of getting lung cancer. Stopping smoking can improve health and decrease risk of cancer.
Health Effects of Asbestos Exposure:
Significant exposure to any type of asbestos will increase the risk of lung cancer, mesothelioma and nonmalignant lung and pleural disorders, including asbestosis, pleural plaques, pleural thickening, and pleural effusions. This conclusion is based on observations of these diseases in groups of workers with cumulative exposures ranging from about 5-1,200 fiber-year/mL. Such exposures would result from 40 years of occupational exposure to air concentrations of 0.125-30 fiber/mL.
Diseases from asbestos exposure take a long time to develop. Most cases of lung cancer or asbestosis in asbestos workers occur 15 or more years after initial exposure to asbestos. Tobacco smokers who have been exposes to aspects have a far greater than additive risk for lung cancer than do nonsmokers who have been exposed meaning the risk is greater than the individual risks from asbestos and smoking added together.
The time between diagnosis of mesothelioma and the time of initial occupational exposure to asbestos commonly has been 30 years or more. Cases of mesotheliomas have been reported after household exposure of family members of asbestos workers and in individuals without occupational exposure who live close to asbestos mines.
Chronic exposure to asbestos may increase the risk of lung cancer, mesothelioma, and nonmalignant lung and pleural disorders.
Asbestosis is a serious progressive, long-term disease of the lungs. Asbestosis is not a cancer. Inhaling asbestos fibers that irritate and inflame lung tissues, causing the lung tissues to scar, causes asbestosis.
The scarring makes it hard to breathe and difficult for oxygen and carbon dioxide pass through the lungs. Asbestosis generally progresses slowly. The latency period for the onset of asbestosis is typically 10-20 years after the initial exposure. The disease can vary from asymptomatic (no symptoms) to disabling and potentially fatal.
Signs and Symptoms of asbestosis include:
1. Shortness of breath (primary symptom)
2. A persistent and productive cough (A cough that experts mucous)
3. Chest tightness
4. Chest pain
5. Loss of appetite
6. A dry, crackling sound in the lungs while inhaling
Pleural Abnormalities- Persons with significant exposure to asbestos are at risk for developing various types of pleural (lining of the chest cavity, outside the lungs) abnormalities. These abnormalities include pleural plaques, pleural thickening, pleural calcification, and pleural mesothelioma.
Mesothelioma is a rare cancer, which may affect the lining of the chest cavity, outside the lung (pleura) or the abdominal contents (peritoneum). Most mesotheliomas are caused by exposure to asbestos.
Lung cancer is a malignant tumor that invades and obstructs the lung’s air passages. Cigarette smoking greatly increases the likelihood of a person developing lung cancer as the result of asbestos exposure. The most common symptoms of lung cancer are cough, wheezing, unexplained weight loss, coughing up blood, and labored breathing.
Other symptoms of lung cancer include shortness of breath, persistent chest pain, hoarseness, and anemia. People who develop these symptoms do not necessarily have lung cancer, but they should consult a physician for advice.
Gastrointestinal and Colorectal Cancers:
Studies of asbestos workers suggest that asbestos exposure might be associated with gastrointestinal (esophagus and stomach) and colorectal (colon and rectum) cancers. However, the evidence is unclear.
Some evidence shows that short-term (acute) oral exposure to asbestos might bring on precursor lesions of colon cancer, and that long-term (chronic) oral exposure might increase the incidence of gastrointestinal tumors.
Kidney, Brain, Bladder, Laryngeal, and Other Cancers:
Results of studies of cancers at other sites are also inconclusive. One reason is that relatively few studies have tried to evaluate the relation between asbestos exposure and non-respiratory cancers.
Some studies have noted excess deaths from, or reported cases, of certain cancers such as the kidneys brain, and bladder. Several epidemiologic studies have reported an increased risk of laryngeal cancer in workers exposed to asbestos.
Mechanisms of Various Health Effects of Asbestos:
When asbestos mineral fibres are inhaled, many of them are deposited on the epithelial surface of the respiratory tree. Entry and deposition of the fibres depend upon the type of fibres and more importantly fibre size (length and diameter) which are important determinants of the health risk posed by asbestos.
The number of fibres that are deposited and the location within the airway where deposition occurs is a function of the aerodynamic properties of the fibres. For typical fibres of chrysotile, amosite and crocidolite, about 30-40% of all the fibres in inhaled air are retained with most of these (about 60%) being deposited in the upper air ways (nose, throat, trachea).
The fibres in the upper airway consist mainly of relatively thick fibres (greater than 3 μm) with thinner fibres being carried deeper into the airways. Most fibres deposited into the airways are removed from the lung by mucociliary transport or by alveolar macrophages (AM), but a small fraction remains in the lung for long periods. In addition, some fibres pass from the lung to the pleura, although the precise mechanism of transport is not known. Those fibres that enter the lymph are presumably able to reach other organs of the body.
Epidemiological surveys and experimental studies established that asbestos is a carcinogen as well as co-carcinogen. Chronic inhalation of airborne asbestos results in the fibrotic lung disease. Deposition of these fibres/particles in the lung is followed by a sequence of events, which starts with change in the free cell population, which includes AM and polynuclear inflammatory cells via their influx.
There have always been debates about the nature of interaction between multiple environmental pollutants in causing diseases to human. Predisposing factors like food preservatives, exposure to cigarette smoke, kerosene soot and bio-fuels at indoor levels would accelerate the disease processes. Cigarette smoke alone has been shown to cause lung cancer but the risk of lung cancer increases substantially due to cigarette smoke in conjugation with exposure to asbestos.
The development of the asbestos industries has always been linked with the recognition of health risk involved. Owing to the growing activities in mining, grinding and manufacturing of asbestos-products, the risk of health hazards has also received wide attention world over.
The sequence of events in the lung, following deposition of fibres includes modulation in the free cell population, primarily characterized by an increase in AM and polymorph nuclear inflammatory cells.
Further, a change in the composition of the lung lining fluids has also been reported. The inflammatory response to these fibres stimulates the release of a variety of inflammatory cell mediators and growth factors which play an important role in the fibrogenesis of the lung.
Approximately 80% of mesotheliomas occur in men exposed to mineral fibres at workplaces and sometimes in their family members or in persons who lives near asbestos sources. Mesothelioma may develop in pleural and peritoneal cavity of the lung.
iii. Peritoneal Mesothelioma:
Peritoneal mesothelioma involves the abdominal cavity, infiltrating the liver and spleen and the bowels pain is the most common presenting complaints. In addition, fluid accumulation in the abdominal cavities, the abdomen appears enlarged, the patient experience nausea, vomiting, swelling of their feet, fever and difficulty in moving their bowels.
iv. Pleural Plaques:
The pleural is a set of thin membrane that lines the chest cavity. Pleura are co-important as they provide lubrication, friction free surface to lung for easily expand and contract against. After an exposure of asbestos for minimum 10 years, pleural changes may begin to appear and these changes may be some times called as pleural thickening, pleural calcification and more commonly pleural plaques. Hyaline plaques of the parietal pleura occur in association with exposure to all types of asbestos. The majority occurs after 20 years or more of the exposure.
This is a typical asbestos-related disease. Asbestos fibres when inhaled and reach in the lung start to damage the lung cells and result is asbestosis (formation of scar tissue in the lung), and/or lung cancer. The risk of lung cancer among people exposed to asbestos is increased by 7 times compared with the general population.
Asbestosis is an interstitial pulmonary fibrosis, which reduces the lung capacity to deliver the oxygen in proper way to the whole body because the lung tissue loses its ability to function. It is characterized by the airway obstruction and air trapping, reducing vital capacity. This disease has relatively long latency period of about 40 years.
Clinically, asbestosis is very similar to interstitial pulmonary fibrosis (IPF). Most patients with well- established asbestosis characterized with shortness of breath, dry cough, and physical examination typically reveals dry rales at the base on inspiration. The usual function changes in the fully developed case are a restrictive defect and decreased diffusing capacity.
vi. Bronchogenic Carcinoma:
Bronchogenic carcinoma is a tumor, arising in tracheobronchial epithelial or alveolar epithelial cells. The average latency period of the disease i.e. the diagnosis of the disease from the time of first exposure to asbestos ranges from 20 to 30 years.
The degree of association varies with the type of mineral fibre, morphology, concentration, exposure regimen, and other predisposing factors like smoking habits or the presence of certain other chemicals, but there is usually a dose- response relation (fiber per cubic centimeter of air times the number of years of exposure). Lung tumor is rare among the mineral fibre workers who do not smoke; although effect of mineral fibres and smoking combines in a multiple fashion to produce lung cancers.
Prevention and Control of Diseases Caused by Asbestos Exposure:
Employers and workers should take appropriate actions to reduce asbestos exposure to below permissible limits.
This can be accomplished by following measures:
1. Exposure Monitoring:
Worker exposure surveys should be made to determine the extent of worker exposure and the effectiveness of engineering controls.
The combined use of detection methods called light microscopy, electron microscopy, and energy dispersive X-ray analysis offer the most accurate approach to identify asbestos and to estimate concentrations that may become airborne upon disturbance.
For the purposes of counting asbestos fibers in these samples, regulatory agencies commonly count as “fibers” those particles of asbestos minerals at least 5 micrometers in length and/with length width ratios of 3:1. For other purposes, such as detecting fibers in bulk building materials, asbestos particles with length: width ratios of 5:1 are counted.
2. Engineering Controls:
The most effective control of airborne concentrations of asbestos fibres is at the source of contamination by enclosure of the operation and/or use of local exhaust ventilation.
Ventilation equipment should be checked to ensure adequate performance. System effectiveness should be checked soon after any change in production, process, or control, which might result in significant, increases in airborne exposure to asbestos fibres.
3. Medical Surveillance:
Pre-placement and annual medical examinations should be made available to all workers who manufacture, use, or handle asbestos.
These examinations should include at least:
(a) Comprehensive work and medical histories to evaluate exposure and signs and symptoms of respiratory disease.
(b) Pulmonary function tests (PFT) including forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1), with calculation of the FEV1/FVC ratio.
Workers with radiographic evidence of asbestosis should be given the opportunity to transfer to jobs without exposure.
4. Work Practices:
Work practices involve both the design of work procedures and the actions of workers.
The following work practices are recommended:
(a) Work procedures should be developed so they do not produce dust.
(b) Work clothes should be vacuumed before removal.
(c) General housekeeping duties should be intensified so that there is no dust accumulation on machinery, beams, comers, and other surfaces. Dustless methods of cleaning such as vacuuming or wetting down should be used. Dry sweeping or blowing with compressed air should be avoided.
(d) Emphasis should also be given to cleanup of spills preventive maintenance, and timely repair of equipment.
5. Personal Protective Equipment (PPE):
Personal protective equipment is not recommended as a primary means of control.
Exposure of workers to airborne asbestos should not be controlled with the use of respirators except:
(a) During installation and implementation of engineering or work practice controls.
(b) In work situations in which engineering and work practice controls are technically not feasible.
(c) During major overhaul and repair of equipment, if exposure to asbestos is possible.
(d) In emergencies.
6. Record Keeping:
The employer must keep an accurate record of all measurements taken to monitor employee exposure to asbestos. This record is to include- the date of measurement, operation involving exposure, sampling and analytical methods used, and evidence of their accuracy; number, duration, and results of samples taken; type of respiratory protective devices worn; name, and the results of all employee exposure measurements. This record must be kept for 30 years.
7. Worker Education:
Workers should be informed of the hazardous nature of asbestos, the results of workplace monitoring and medical tests, and the correct usage and maintenance of respirators.
8. Labeling of Asbestos Containers:
Packaged asbestos should be labeled correctly, and health warnings should be placed on each container to alert users and handlers as well as producers to the hazards of asbestos.
EPA = Environmental Protection Agency; IARC = International Agency for Research on Cancer; NIOSH = National Institute of Occupational Safety and Health; OSHA = Occupational Safety and Health Administration; PEL = permissible exposure limit; REL = recommended exposure limit; TLV = threshold limit value; TWA = time-weighted average; IFA = Indian Factories Act, 1948 f = fibres.
9. Hygiene Facilities and Practices:
Clean change rooms must be furnished by employers for employees who work in areas where exposure is above the TWA and/or excursion limit. Showers must be furnished so that employees may shower at the end of the work shift. Lunchroom facilities for those employees must have a positive pressure, filtered air supply and should be readily accessible to employees. Employees must wash their hands and face prior to eating, drinking or smoking.
Researchers from Netherlands have demonstrated the safety of a potential vaccine against mesothelioma, a rare cancer associated primarily with asbestos exposure. The vaccine, which infuses uses a patient’s own dendritic cells (DC) with antigen from the patient’s tumor, was able to induce a T-cell response against mesothelioma tumors.
Example 6 # Environmental Hazards of Pesticides:
Besides being beneficial for increased crop yield as well as in vector control programme, a pesticide has resulted in several health-related problems. Unintended exposure to pesticides can occur during their manufacturing, formulation and application or from environmental residues after application.
Pesticides have been an integral part of modern agriculture and until very recently, not much attention was given to the potential problem of environmental and groundwater contamination. Indiscriminate and injudicious use of chemical pesticides, in agriculture has resulted in several associated adverse effects such as environmental pollution, ecological imbalances, pesticides residues in food, fruits and vegetables, fodder, soil and water, pest resurgence, human and animal health hazards, destruction of bio control agents, development of resistance in pests etc.
Pesticides, which are toxic to pests, might produce some adverse health effect. Nine of the twelve most unwanted persistent organic pollutants (POP’s) are pesticides used in agriculture crops and for public health vector control programme. These twelve POP’s have been identified as a powerful threat to the human and wildlife health on a global basis.
A pest has characteristics that are regarded by human as injurious or unwanted. The term pesticide covers a wide range of compounds including insecticides, fungicides, herbicides, rodenticides, molluscicides, nematocides, plant, growth regulators and others, Ideally a pesticide must be lethal to the targeted pests, but not to non target species, including man.
Pesticides can be classified on the basis of type of pest control toxic property and chemical composition.
On the basis of pest control:
(i) Insecticides (against insect pest)
(ii) Herbicides (for killing and controlling weeds)
(iii) Fungicides (against fungal diseases)
(iv) Others (e.g. molluscicides, nematocides, etc.)
On the basis of their acute toxicity:
Class Ia- Extremely hazardous, demarcated in red.
Class Ib- Highly hazardous, symbolized by a yellow triangle.
Class II- Moderately hazardous, marked by a blue triangle.
Class III- Slightly hazardous.
On the basis of chemical composition:
(i) Organophosphate compounds
(iii) Synthetic pyrethroids
Production and Consumption of Pesticides:
Use of pesticides in India began in 1948 when DDT was imported for malaria control and BHC for locust control. India started pesticide production with manufacturing plant for DDT and benzene hexachloride (BHC) in the year 1952.
The introduction of other synthetic insecticides organophosphate (OP) insecticides in the 1960s, carbonates in 1970 and pyrethroids in 1980s and the introduction of herbicides and fungicides in 1970s- 1980s contributed greatly in pest control and agricultural output.
The following working condition of farmers makes them susceptible to high exposure to pesticides:
(i) Safety gears costly and also not suitable for tropical climate.
(ii) Practice Poor to dangerous.
(iii) Barefoot and barehanded, wearing minimum cloth, leaking spray tank etc.
(iv) Mixing of concentrated chemicals and refilling spraying tanks and spraying even tasting the mixture.
(v) Multiple pesticides used mix and match subsequent medical management difficult.
(vi) Unintended exposure of women and children to pesticides while mixing and spraying.
Health Effects of Pesticides:
i. Organophosphorus Insecticides:
Organophosphorus insecticides are normally esters, amides or thiol derivatives of phosphoric, phosphonic, phospnorothioic, or phosphonothioic acids. Most Organophosphorus insecticides are more stable in the pH range that may be encountered in the environment (pH 3.6) than at neutral pH. Different climatic conditions, especially temperature and humidity, before, during, and after spraying may influence the survival time of insects.
The metabolic fate of Organophosphorus insecticides is basically the same in insects, animals, and plants. Uptake in animals and insects may occur through the skin, respiratory system, or gastrointestinal tract. Metabolism occurs principally by oxidation, hydrolysis or by conformational changes by transfer of a group of the molecule.
The signs and symptoms of acute organophosphate poisoning are an expression of the effects caused by excess acetylcholine (cholinergic syndrome).
According to the degree of the severity of poisoning, the following signs and symptoms can occur:
Mild anorexia, headache, dizziness, weakness, anxiety, sub-sternal discomfort, fasciculation of the tongue and eyelids, miosis and impairment of visual acuity.
Moderate nausea, salivation, bronchorrhoea, lacrimation, abdominal cramps, diarrhea, vomiting.
Sweating, hypertension or hypotension, and muscular fasciculation.
Severe miosis or mydriasis, non – reactive pupils, dyspnoea, respiratory depression, pulmonary oedema, cyanosis, loss of sphincter control, convulsions coma, bradycardia or tachycardia, cardiac ischaemia, cardiac dysrhythmias, hypokalaemia, and hyperglycaemia. Acute pancreatitis has also occurred. Muscular paralysis may involve the respiratory muscles. Some organophosphorus pesticides have causes delayed peripheral neuropathy.
ii. Organochlorines (OC):
Organochlorines are compounds that contain carbon, chlorine and hydrogen. Their chlorine – carbon bonds are very strong which means that they do not break down easily. They are highly insoluble in water, but are lipophilic.
The organochlorines compound exhibit an ability to resist degradation, associate with sediments and to accumulate in the tissue of invertebrates, fish and mammals. Most of the organochlorine compounds have properties that contribute to their ability to concentrate in biota and magnify in the food chain.
Organochlorines contribute too many acute and chronic illnesses. Symptoms of acute poisoning can include tremors, headache, dermal irritation, respiratory problems, dizziness, nausea, and seizures. Organochlorines are also associated with many chronic diseases.
Studies have found a correlation between organochlorine exposure and various types of cancer, neurological damage (several organoclorines are known neurotoxins). Parkinson’s disease, birth defects, respiratory illness, and abnormal immune system function.
Many organochlorines are known or suspected hormone disruptors, and recent studies shows that extremely low levels of exposure in the womb can cause irreversible damage to the reproductive and immune systems of the developing fetus.
Carbamates, or urethanes, are a group of organic compounds sharing a common functional group with the general structure – NH(CO)O-. Carbamates are esters of carbamic acid, NH2COOH, an unstable compound. These insecticides can cause cholinesterase inhibition poisoning by reversibly inactivating the enzyme acetylcholinesterase.
Health hazards for man occur mainly from occupational over-exposure to carbamate insecticides resulting in poisoning characterized by cholinergic symptoms caused by inhibition of the enzyme ACHe. The main routes of exposure are inhalation and skin. Apart from the symptoms indicative of ChE poisoning, other signs and symptoms induced by certain carbamates are skin and eye irritation, hyperpigmentation, and influence on the function of testes (sight increase of sperm abnormalities).
Pesticides as Endocrine Disruptors:
An endocrine disruptor is an exogenous substance or mixture that after functions(s) of the endocrine system and consequently causes adverse health effects in an intact organism or its progeny or sub populations. Exposure to low doses of endocrine-disrupting chemicals may have little effects on the exposed adult.
Population estimates are preliminary and based on an ongoing assessment of polluted sites estimated global impact is extrapolated from current site research and assessment surveys organism, but the offspring of that organism may suffer drastic repercussions.
Another group of pesticide i.e. pyrethroid compounds, which are considered to be safe till recently as compared to organochlorine and organochlorine compounds have also been reported to be able to disrupt estrogen function in vitro.
Exposure to some of the pesticides during infancy, even at very low levels, can lead to serious life-long consequences if the pesticides disrupt hormone – driven development processes.
i. Integrated Pest Management (IPM):
IPM is an eco-friendly approach, which encompasses cultural, mechanical, biological and need based chemical control measures.
The IPM approach is being disseminated through various schemes/projects at national and state level with the following objectives:
(i) To maximize crop production with minimum input costs.
(ii) To minimize environmental pollution soil, water and air due to pesticides.
(iii) To minimize occupational health hazards due to chemical pesticides.
(iv) To preserve ecosystem and maintain ecological equilibrium.
(v) To no or less use of chemical pesticides for minimum pesticide residues.
The pesticide misuse should be minimized to reduce the exposure.
The pesticide misuse includes:
(i) Failing to follow label or permit instructions.
(ii) Using pesticides in a way that is likely to injure people or damage property.
(iii) Harming a non-target plant or animal.
(iv) Storing pesticides in container that do not have that approved label attached.
(v) Disposing of a pesticide or its container illegally e.g. pouring pesticide waste down a drain.
(vi) Spraying pesticides from an aircraft without a relevant license.
(vii) Spraying pesticide against the wind direction.
(i) When using pesticides always read the pesticide container label before use and strictly follow the directions for use provided by the manufacturer or supplier.
(ii) Prepare pesticides in a well – ventilated area, where appropriate protective clothing (such as gloves, facemask and goggles) and keep children and animals away from preparation and application area.
(iii) Prepare only enough pesticide for the particular application, use all the prepared pesticide on the application site (but avoid excess application), and avoid using pesticides on windy days.
(iv) Persistent organochlorine pesticides should be not be as these chemicals are not readily broken down in the environment and accumulate in humans and animals and therefore have the potential to harm human health and the environment many years after application.
(i) NEVER store pesticides in non-pesticide containers, e.g. containers used or labeled for food and drink.
(ii) NEVER re-use pesticide containers for any purpose other than to hold the original pesticide.
(iii) NEVER dispose of pesticide wastes down drains, toilets, sinks, gully traps or into bodies of water (such as rivers, lakes, streams or dams).
(iv) NEVER dispose of pesticide wastes or contaminated or un-cleaned pesticide containers in public jitter bins or private garbage bins, or leave them out for curbside collection.
(v) NEVER dispose of surplus pesticides in the garden.
(vi) NEVER deliver used glass or plastic pesticide containers to bottle collection depots.
(vii) NEVER burn pesticide wastes, including pesticide containers.
If pesticides are spilled on the skin:
(i) Follow the first-aid directions on the label – or immediately wash with soap and water.
(ii) Remove pesticide contaminated clothes immediately wash them separately from other clothes.
(iii) Monitor for symptoms of poisoning if in any doubt, seek immediate medical attention.
(iv) If pesticides come in contact with the eyes, wash with copious amounts of water.
iii. Use of Bio-Pesticides:
Bio-pesticides are a group of pesticides derived from natural materials like animals, plants, bacteria, and certain minerals. For example, canola oil and baking soda have pesticidal applications and are considered bio-pesticides. Bio-pesticides fall into three major classes.
1. Microbial pesticides consist of a microorganism (e.g., a bacterium, fungus, virus or protozoon) as the active ingredient.
2. Plant-incorporated-Protectants (PIPs) are pesticidal substances that plants produce from genetic material that has been added to the plant.
3. Biochemical pesticides are naturally occurring substances that control pests by non-toxic mechanisms.
Bio-pesticides are usually less toxic than conventional pesticides.
(i) Bio-pesticides generally affect only the target pest and closely related organisms, in contrast to broad spectrum, conventional pesticides that may affect a group of organisms such as birds, insects, and mammals.
(ii) Bio-pesticides often are effective in very small quantities and often decompose quickly, thereby resulting in lower exposures and largely avoiding the pollution problems caused by conventional pesticides.