Environmental Pollution- A detriment to a healthy society
Man has tried to change the environment in different ways from the days when he was a cave dweller. Any substance present in the environment, which may produce abnormality in metabolism or alter the well being of organism, is called an environmental pollutant.
A poison is a substance which causes death or harm if introduced in the living body or brought into contact with parts of the body. Lethal doses (per kg body weight) of some toxic substances are: Cyanide = 1 mg/kg body weight; Morphine = 25 mg/kg; Aspirin = 500 mg/kg; Ethyl alcohol = 10 g/kg.
CORROSIVES These are strong acids (sulfuric acid, hydrochloric acid); strong alkalies (sodium hydroxide, ammonia); and salts (zinc chloride, potassium chromate).
They remove water from the tissues, coagulate the cellular proteins and convert hemoglobin into acid hematin. The cause of death is circulatory collapse and spasm of glottis.
Sulfuric acid can be detected from the gastric fluid by reacting with barium chloride to produce a white precipitate of barium sulfate. Ammonia, potassium hydroxide, sodium hydroxide, calcium hydroxide and ammonium carbonate are the common alkalies encountered.
They remove water from the tissues and precipitate proteins. These can be detected in the gastric juice by reacting with silver nitrate to form silver hydroxide, which forms a brown precipitate.
Ammonia is highly neurotoxic.
Cyanide Poisoning Cyanide causes tissue anoxia by chelating the ferric ions of the intracellular respiratory enzyme, cytochrome oxidase. Poisoning may be due to suicidal attempts.
Industrial exposure may occur in the persons working with hydrocyanic (prussic) acid or with potassium cyanide. Ingestion of amygdalin, present in kernels of certain fruits (apricots, almonds, peaches) is also a common cause. Dicobalt edetate (kelocyanor) is the antidote, which chelates the cyanide.
Another method is to give sodium nitrite and sodium thiosulfate intravenously. The nitrite converts hemoglobin to methemoglobin. Ferric ion of Met-Hb takes up cyanide as cyan-met-hemoglobin so that cytochrome oxidase is now free of cyanide. Later thiosulphate detoxifies the cyanide by forming thiocyanate, which is excreted. But in practice, death is instantaneous and time may not be available for the treatment.
IRRITANTS Important chemical irritants are phosphorus, chlorine, bromine and iodine. Metallic irritants are arsenic, antimony, mercury, copper, lead, zinc and silver. Organic irritants from plants include castor, croton, and calotropis. Phosphorus It is a poison affecting cellular oxidation.
Accidental poisoning in children may occur due to chewing of fireworks or rat poisons. Symptoms resemble acute liver disease. The poison is oxidized in the body. Neurotoxins These may act at cerebral level, e.g. opium, alcohol, ether, chloroform, datura, belladona, cannabis, etc. Those acting at spinal level are aconite, quinine and oleander.
HEAVY METAL POISONS
1. Lead Poisoning A 61-year old male was admitted in a medical college hospital in Bengaluru with typical symptoms of lead poisoning (encephalopathy, nephropathy and anemia).
The lead level in blood was over 100 microgram/dl. On detailed questioning, the patient told that he was very particular to take only “pure food” and he was preparing fresh “aatta” (wheat flour).
He was powdering wheat on a small hand-mill at his house. The machine had a crusher which was fixed on the pivot by soldering with lead. So for the last 30 years, he was getting daily doses of lead along with his “pure aatta”.
The company had already supplied thousands of such instruments throughout the country. All those families might be getting harmful doses of lead! 1-A. Sources of lead poison
i. Lead is the most common environmental poison in India. About 30% of population are already affected by lead poisoning. It is dispersed into air, food, soil and water.
Lead poisoning is also included in the class of “summer disease”, as increased temperature brings out the dust, and lead particles will also be in the air
ii. Paint is the major source for exposure, especially in children, as they bite painted toys. US law states that paints should not contain more than 0.06% of lead.
But Indian paints, especially cheaper ones may contain up to 30% lead salts. Paint is peeled off as small flakes from walls of living rooms.
iii. Increased content of lead is seen in air, water and vegetables in cities and near highways. This is due to the tetraethyl lead derived from the exhaust of vehicles. Statutory use of lead-free petrol has reduced this type of contamination.
iv. Lead pipes are important sources for contamination.
v. Newspapers and xerox copies contain lead, which is adsorbed to fingertips, and later contaminate foodstuff taken by hands.
vi. One pack of cigarette contains 15 microgram of lead and chronic smokers have higher blood levels of lead.
vii. Lead chromate is commonly used as adulterant in curcumin.
viii. Battery repair, radiator repair, soldering, painting and printing are occupations prone to get lead poisoning. 1-B.
Signs and Symptoms of Lead Poisoning
i. Lead is a cumulative poison and is accumulated in tissues over the years. It is not biodegradable. 90% of lead is seen in bones, 9% in blood and 1% in brain and kidneys.
ii. There is no “safe” level in blood; about 10 mg/ dl can be tolerated. More than 10 mg/dl in children and more than 25 mg/dl in adults leads to toxic manifestations.
iii. Lead can pass through placenta and milk. Miscarriage, still birth, and premature birth are reported in lead poisoning of mothers.
iv. Developing brains are more susceptible to lead. Permanent neurological sequelae, cerebral palsy and optic atrophy may be seen. v. In children, mental retardation, learning disabilities, behavioral problems, hyperexcitability and seizures are seen.
Even 10 microgram/dl of lead in blood for a long time will reduce I.Q. to 8 points. vi. Anemia, abdominal colic and loss of appetite are very common. vii. If the blood level is more than 70 mg/dl, acute toxicity is manifested, as encephalopathy, convulsions, mania, neuropathy, abdominal colic, severe anemia and kidney damage.
Discoloration and blue line along the gums are characteristic features of acute lead poisoning. viii. Lead inhibits heme synthesis.
Basophilic stippling of red cells are seen in the peripheral blood and bone marrow smears. This is due to the agglutination of ribosomes. Globin synthesis is adversely affected. Lead particularly inhibits delta amino levulinic acid (ALA) synthase and ALA-dehydratase.
Lead also inhibits the enzyme ferrochelatase. Life span of RBC is shortened. Anemia enhances lead absorption, lead in turn produces more anemia; thus a vicious cycle is operating.
Lead will inhibit absorption of iron and calcium. 1 molecule of lead will inhibit absorption of 1000 molecules of calcium. 1-C. Treatment of Lead Poisoning Calcium dodecyl edetate (Calcium disodium versenate), penicillamine and dimercaprol (BAL) are used as antidotes.
Dimercaptosuccinic acid is a better but costly antidote.
2. Mercury Poisoning It is the most common industrial poison. The source for poisoning may be elemental, inorganic or organic mercury. 2-A.
Elemental mercury Hazard may come from inhalation of mercury vapor from broken thermometers, sphygmomanometers orfrom dental amalgam. In acute poisoning pulmonary edema and encephalopathy may result.
A classical triad of (a) oral lesions (gingivitis, salivation and stomatitis), (b) tremor and (c) psychological changes (insomnia, shyness, emotional instability, memory loss) are the hallmark of chronic elemental mercury poisoning. This is called erethism. 2-B.
Inorganic Mercury Poisoning may arise from calomel (cathartic), topical medicines and in plastic industry.
Acute effects include gingivitis, gastritis, vomiting and pulmonary edema. In chronic cases, erethism, especially the neuropsychiatric manifestations predominate. 2-C. Organic Mercury Poisoning may occur from paints, fungicides and cosmetics. From mercury salt wastes, the bacteria synthesise methyl mercury (CH3–Hg+). This then enters into the fish. Eating of such fish is the most common cause for organic mercury poisoning.
In 1953, in Minamata Bay, Japan, industrial effluent caused methyl mercury poisoning, an epidemic lasting for several years. Organic mercury poisoning is thereafter called Minamata disease.
The classical triad of methyl mercury exposure is dysarthria, ataxia and visual field constriction. In severe cases, toxic encephalopathy, sensory neuropathy, intention tremor, hearing loss and spasticity may also be seen. Laboratory investigation findings are: i. Normal level of mercury in blood is less than 1 mg/dl. When it is increased to 2-5 mg/dl, symptoms of toxicity appear. A level of 15 mg/ dl is fatal. ii. Urinary excretion of mercury is elevated, especially in chronic poisoning. iii. Hair analysis can detect organic mercury compounds.
Dimercaprol derivatives, D-penicillamine, and N-acetyl cysteine can increase the excretion of mercury and are useful in treatment.
3. Aluminium Toxicity i. Aluminium is the third most abundant element after oxygen and silicon in earth’s crust. Exposure is from packing and building materials, paint pigments, insulating materials, cosmetics, antacids, and aluminium cooking vessels. ii.
An average Indian consumes 1-10 mg of aluminium per day, but only part of it is absorbed. Tolerable upper limit of absorption is 1 mg/day. Only up to 100 microgram/day can be eliminated through urine. If intake is more than 100 mg/day, toxicity results. iii. Aluminium stimulates production of free radicals. It prevents absorption of calcium, phosphorus and iron.
It also interferes with heme synthesis. iv. Aluminium precipitates Alzheimer precursor proteins and may lead to Alzheimer’s disease. Aluminium is implicated in degeneration of dendrites.
It is also involved in Parkinson’s disease. v. Osteomalacia and microcytic hypochromic anemia are other manifestations of toxicity.
4. Arsenic Toxicity The oxides of arsenic are commonly used as fruit sprays, pesticides, rat poisons, etc. It acts on sulfhydryl enzymes and interferes with cell metabolism. It may also cause intravascular hemolysis, which leads to hemoglobinuria.
The trivalent or pentavalent organic arsenic compounds are less toxic than inorganic compounds. The symptoms are anaphylactic reactions or later development of agranulocytosis, hepatitis, jaundice and encephalitis.
PESTICIDES AND INSECTICIDES DDT (dichlorodiphenyl trichloro ethane) It is fat soluble and deposited in the adipose tissue. It is not excreted. Thus concentration inside the body goes on increasing.
The DDT used in North America as pesticide during 1970s has reached Antarctica and reduced the thickness of shell of eggs of penguins. Even though DDT is banned in many countries, it is still available in India.
Many antifungal agents sprayed on fruits are having long term effects of depressed spermatogenesis and fertility. Organophosphorus Compounds Organophosphorus (ORP) and organocarbamates (ORC) are the common pesticides and organo sulfur compounds (dithiocarbamates) are fungicides. Organophosphorus compounds, Parathion and Malathion are powerful neurotoxic agents.
They inhibit acetyl choline esterase through phosphorylation of the active center of the enzyme. Hence acetylcholine accumulates in the nerve endings. Thus the transfer of nerve impulse across synapses and at the nerve-muscle junction is prevented.
Diagnosis depends on the estimation of cholinesterase in serum and RBC. The antidote is atropine sulfate and cholinesterase re-activators (diacetyl monoxime or pralidoxime).
OCCUPATIONAL AND INDUSTRIAL HAZARDS Polychloro-biphenyls They are widely used in various industries, can mimic thyroid hormones. Bisphenols from plastic containers leach out into drinking water. Vinyl phenols are dissolved from PVC pipes.
These chemicals will lead to decrease in fertility and alteration in behavior. Freon and Chlorofluoro Methane CF2Cl2 (CFC) and CFCl3 are used in refrigerators and spray-cans. They are photo-dissociated to chlorine atoms. When chlorine reaches upper atmosphere, it destroys the ozone layer that has been protecting the biosphere against excessive radiation, ever since life emerged. Methanol It is the organic solvent widely used in paints and anti-freezes.
It may be consumed in place of ethanol as a substitute. Alcohol dehydrogenase converts methanol to formaldehyde. It is more toxic than ethanol. Optic neuritis and blindness is the characteristic toxicity. The treatment is to give large doses of ethanol, which is preferentially oxidized in the body so that formaldehyde formation is reduced.
AIR POLLUTANTS The atmosphere contains mostly nitrogen (78.09%) and oxygen (20.94%), carbon dioxide (0.03%), and water vapor. The permissible level of total suspended particles (TSPs) is 230 mg/cu.m. A chemical other than those conventionally accepted in the composition of clean air is called a Contaminant. A contaminant that occurs in the atmosphere in sufficiently high concentrations to cause an adverse effect is called a Pollutant.
The main natural sources of pollution are due to volcanic eruption, forest fires, dust storms and air borne particles. In addition to dissolved gases, suspended particulate matter like dust and soot, also adds to the contamination of air. They range in size from 1 to 10 microns in diameter. The major artificial sources of pollution arise due to emissions from automobiles, industry and power plants. These are carbon dioxide, carbon monoxide, hydrocarbons, oxides of nitrogen, oxides of sulfur and lead.
The poisonous mixture of smoke, fog, air and other chemicals is called smog. The chemically reducing smog is derived from the combustion of coal and oil, and contains sulfur dioxide (SO2), sulfur trioxide (SO3), mixed with soot. SO2 and SO3 in presence of atmospheric water vapor, become sulfurous and sulfuric acids, respectively.
This is the precursor of acid rain that may be carried by wind to long distances. Chronic respiratory symptoms are associated with sulfur oxide or particulates in air. Exacerbations of bronchitis were associated with high concentrations of smoke and sulfur oxide.
Children living in polluted areas show diminished ventillatory function when compared with their counterparts living in less polluted areas. Heart diseases are also related to pollutants such as ozone, sulfur dioxide, sulfates and cadmium in the air. High level of carbon monoxide decreases ability to concentrate and decreases visual threshold.
Inhalation of air borne lead can cause neurological disturbances. Industrial Pollution Dramatic and disastrous episodes of air pollution have been documented in many industrialized centers in the world. An example was the London Fog of 1952, in which approximately 4000 deaths occurred over a period of 2 weeks, following 5 days of severe cold and dense fog.
Another such event was the Bhopal gas tragedy in December 1984 which claimed thousands of lives due to methyl isocyanate (MIC) poisoning.
Passive Cigarette Smoking The particulate load in a household is directly proportional to the number of cigarette smokers living at home. Increased prevalence of respiratory illnesses and reduced levels of pulmonary function measurements have been found in children of smoking parents.
Studies have also concluded that lung cancer risk is higher in non-smokers who live under the same roof with smokers.