Environmental Medicine: An Introduction

Emory University - Rollins School of Public Health
Atlanta, Georgia

Instructor(s): Frumkin, Howard
Subject area: Health / Medicine
Department: Public Health
Level: Undergraduate Medical
Number of participants: 90
Duration of exercise: 90 minutes
Cost/equipment needed: None
Learning objective: Provide Information
Teaching style: Passive Learning

Please note that the copyright for this course project is retained by the instructor.

This lecture is presented to first year medical students at Emory University as part of their Patient/Doctor Course. The lecture provides a broad overview of environmental medicine beginning with a discussion of exposure, health effects and how to think about the possible links between the two. The role of physicians in this field is also discussed. Several examples of environmental hazards are discussed in detail, including a hazardous waste site, lead contamination, air pollution, multiple chemical sensitivity, and global climate change. A list of suggested readings is included for each hazard.

I. How to think about the health effects of environmental exposures

A. Think about the exposure
1. What is it?
2. How much is there?
3. What is the pathway to people?

B. Think about the health effect
1. What is it?
2. How much of it is occurring?

C. Are the exposure and the health effect linked?

D. What should the physician do?
1. Diagnosis and treatment
2. Advice to your patients and the community
3. Prevention

II. Some specific situations

A. A hazardous waste site

B. Lead contamination

C. Air pollution

D. Multiple chemical sensitivity

E. Global warming

(A local article about and illegal hazardous storage site is included here)

I. The exposures

A. Over the years huge amounts of hazardous wastes have been generated by industry and private citizens. The U.S. continues to produce approximately 275 million tons of hazardous waste annually, just over one ton per person.
B. Although these wastes can be treated, most have been dumped or left behind. The EPA currently lists approximately 40,000 uncontrolled hazardous waste sites, of which approximately 1,500 are "Superfund" sites eligible for cleanup with federal funds.
C. Of these sites approximately 48% are abandoned waste storage/treatment/recycling sites, 33% are abandoned manufacturing facilities, 4% are government facilities (military bases, weapons complexes), 4% are mines, and 11% fall into other categories.
D. A wide range of toxic materials are found in hazardous waste sites:
Metalslead, arsenic, mercury
VOCstrichloroethylene, toluene, benzene, chloroform,
tetrachloroethylene, 1,1,1-trichloroethane
methylene chloride, ethylbenzene, xylene, vinyl
chloride, carbon tetrachloride
Halogenated pesticides and related compoundsDDT, PCBs
Biological wastes

E. These materials can reach people through a variety of routes: INSERT FIGURE 56.1 FROM SULLIVAN AND KRIEGER P 619

II. The health effects

A. Concern and alarm in the community
B. Acute toxicity
C. Reproductive toxicity
D. Immunotoxicity
E. Skin rashes
F. Cancer
G. Neurotoxicity

Further reading:
Andrews JS, Frumkin H, Johnson BL, et al. Hazardous Waste and Human Health: International Congress on the Health Effects of Hazardous Waste. Princeton: Princeton Scientific Publishing, 1994.
National Research Council. Environmental Epidemiology: Public Health and Hazardous Wastes. (Washington: National Academy Press, 1991).
Griffith J, Duncan R, Riggan W, Pellom A. Cancer mortality in U.S. counties with hazardous waste sites and ground water pollution. Arch Environ Health 1989;44:69-74.
Geschwind S, Stolwijk J, Bracken M, et al. Risk of congenital malformations associated with proximity to hazardous waste sites. Am J Epidemiol 1992;135:1197-1207.
Ozonoff D, Colten ME, Cupples A, et al. Health problems reported by residents of a neighborhood contaminated by a hazardous waste facility. Am J Ind Med 1987;11:581-97.

(A local article on lead found in the soil of school grounds is included)

I. The exposure

A. Lead is a heavy metal. It is found naturally with other metals such as copper, and when mined it is used in a wide range of applications: batteries, bullets, printing, paint (formerly), gasoline (formerly), and others.
B. Adults can be exposed at work (smelters, battery plants, welding, etc.) or through recreational activities (stained glass, firing ranges, lead sinkers). Children can be exposed through eating paint, playing on contaminated soil, or exposure to their parents' work clothes.
C. Routes of absorption include ingestion and inhalation.
D. The amount of lead a person has absorbed is reflected by the blood lead level, measured in mcg/dL. The CDC's level of concern is 10 mcg/dL, OSHA's permissible level for workers is 40-50 mcg/dL, and levels above 70 or 80 mcg/dL cause acute toxicity.

II. The health effects

A. Neurologic system
B. Blood
C. Renal toxicity
D. Gastrointestinal symptoms
E. Reproductive toxicity

Further reading:
CDC. Preventing Lead Poisoning in Young Children. Atlanta: Centers for Disease Control, 1991.
Cullen MR, Robins JM, Eskanazi B. Adult inorganic lead intoxication: presentation of 31 new cases and a review of recent advances in the literature. Medicine 1983;62:221-47.
Or read the lead chapters in any of the major environmental and occupational health textbooks:
Sullivan and Krieger, Hazardous Materials Toxicology: Clinical Principles of Environmental Health (Baltimore: Williams and Wilkins, 1992).
Rosenstock and Cullen. Textbook of Clinical Occupational and Environmental
Medicine (Philadelphia: Saunders, 1994).
Rom, Environmental and Occupational Medicine (Second Edition) (Boston: Little, Brown, 1992).
Brooks, Environmental Medicine (St. Louis: Mosby, 1995).


A 36-year-old woman presents to her family practitioner in Atlanta concerned about her asthma. She explains that she had asthma for a few years in childhood, but this resolved spontaneously. Eight years ago she moved to Mexico City for two years, where she worked as a journalist. Her asthma returned and became fairly severe. After returning to the U.S., she lived in Phoenix, and had no further problems. However, she moved to Atlanta last year, and has had episodes of wheezing, especially during the summer. She is also concerned because her four-year-old son seems to have asthma. She wonders whether Atlanta's atmosphere may be contributing to their problem, and what advice you would give her.

I. The exposure: "criteria" pollutants that the EPA must regulate, as required by the 1970 Clean Air Act :

A. Ozone: a "secondary pollutant" not emitted directly but formed by the reaction of hydrocarbons and oxides of nitrogen (NOx) in the presence of sunlight. Common where motor vehicles are common, since they release both constituents. A respiratory irritant that impairs lung function and causes and/or aggravates several kinds of lung disease.
B. Carbon monoxide: A byproduct of incomplete combustion from cars, generators, etc. Usually doesn't accumulate except in closed spaces. Binds with hemoglobin, causes cellular asphyxia.
C. Sulfur dioxide: A byproduct of burning sulfur-containing fossil fuels, mostly at power plants and other industrial facilities. A principal cause of acid rain. Found together with particulates, hence the term "acid aerosols." Soluble in water, so it forms sulfurous and sulfuric acid on contact with mucous membranes. This causes mucous membrane irritation and impaired mucociliary clearance, and exacerbates asthma.
D. Particulates: Dust, soot, smoke, and certain chemicals such as oxides of silicon and iron. Sources include motor vehicles, factories, power plants, wood burning. The smaller particles bypass the respiratory defenses and reach the lower airways. Higher particulate levels correlate with more respiratory symptoms and higher mortality.
E. NOx: Nitrogen oxide (NO) and nitrogen dioxide (NO2) are produced by high-temperature combustion in car engines, energy plants, and factories, from oxygen and nitrogen naturally in the air. Also produced by microbial action, volcanoes. Combines with water to form nitric and nitrous acids. Toxic to airways but less so than ozone.
F. Lead: See above. Much less of a problem as an air pollutant since it was removed from gasoline in the mid-1970s.
G. Hydrocarbons: These are volatile organic compounds (VOCs) from gasoline, industrial production, and the use of solvents.

II. The health effects

A. Acute, high-dose exposures as in Meuse River Valley, Belgium (1930), Donora, Pennsylvania (1948), London (1952): thousands of sick people (cough, shortness of breath, headaches, vomiting, burning eyes, running noses) and many excess deaths, mostly among the elderly or those with underlying heart or lung disease.
B. Chronic, lower-level exposures: Irritation of eyes, nose, throat by sulfur oxides, acid aerosols.
C. Asthma: Increased pollution levels (both particulates/acid aerosols and ozone) are associated with asthma exacerbations. This is notable since asthma prevalence, hospitalization rates, and mortality are all increasing.
D. Acute respiratory infections: In both children and adults, infections such as bronchitis and pneumonia are associated with higher levels of several pollutants, including SO2, NO2, and ozone.
E. Chronic obstructive pulmonary disease: Although smoking is the major cause of COPD, air pollutants (especially SO2 and particulates) can probably also cause it and can clearly exacerbate it.
F. Mortality: In large cities with variations in air pollution levels, mortality increases one or two per cent on polluted days, and declines one or two per cent on especially clean days. The major factor seems to be particulates.

Further reading:
Rusznak C, Devalia JL, Davies RJ. The impact of pollution on allergic disease. Allergy 1994; 49 (Suppl 18): 21-7.
Barnes PJ. Air pollution and asthma. Postgrad Med J 1994; 70: 319-25.
Neher JO, Koenig JQ. Health effects of outdoor air pollution. Am Fam Physician 1994; 49: 1397-404, 1407-08.
Gong H. Health effects of air pollution: a review of clinical studies. Clin Chest Med 1992; 13: 201-14.
Bates DV. Adverse health impacts of air pollution -- continuing problems. Scand J Work Env Health 1995; 21: 405-11.


"Doctor, I was doing fine, a healthy and high-functioning sales representative, until a couple of years ago. I used to jog every day, and was never sick! But then one day, they were cleaning the heating system in my building, and a big puff of some chemical was blown right through the vent near my desk. I smelled a strong smell, felt dizzy, and felt like my throat had shut and I couldn't breathe. I barely made it out of the building, and went home, where I had to sleep for two days. As soon as I came back to the building I smelled the same smell, and felt dizzy and confused. This went on for several weeks until they moved me to a different part of the building. Whenever I went back to my old office I felt the same way, and I started getting skin rashes and having nausea and diarrhea too. After a few months it seemed to happen in other places: when I would smell fresh paint, when I should smell perfume, when I would smell gasoline. When I had new carpet installed in my living room I could smell it and I was sick for three weeks! I had to have the carpet removed. I couldn't keep working, and now I stay at home all the time, without much of a social life. I have removed all the chemicals from my home, but I'm still not well."

I. Definitions

A. Ecologic illness is a polysymptomatic, multisystem chronic disorder manifested by adverse reactions to environmental excitants, as they are modified by individual susceptibility in terms of specific adaptations. The excitants are present in air, water, drugs, and our habitats. (Clinical Ecology)
B. An acquired disorder characterized by recurrent symptoms, referable to multiple organ systems, occurring in response to demonstrable exposure to many chemically unrelated compounds at doses far below those established in the general population to cause harmful effects. No single widely accepted test of physiologic function can be shown to correlate with symptoms. (Cullen) This definition implies seven major diagnostic features:
1. The disorder is acquired in relation to some documentable environmental exposure(s), insult(s), or illness(es).
2. Symptoms involve more than one organ system.
3. Symptoms recur and abate in response to predictable stimuli.
4. Symptoms are elicited by exposures to chemicals of diverse structural classes and toxicologic modes of action.
5. Symptoms are elicited by exposures that are demonstrable (albeit low).
6. Exposures that elicit symptoms must be very low, i.e. standard deviations below "average" exposures known to cause adverse human responses.
7. No single widely available test of organ function can explain symptoms.

II. History

A. 1881: "American nervousness" or "neurasthenia" (G.M. Beard): Features included "special idiosyncracies in regard to food, medicines, and external irritants." Primary cause ascribed to modern civilization, which was distinguished from the ancient by five characteristics: steam-power, the periodical press, the telegraph, the sciences, and the mental activity of women.
B. 1930's-40's: The concept of food allergy was extended to include a causative role in chronic diseases of unknown etiology such as rheumatoid arthritis, ulcerative colitis, and migraine headache. Food allergy was also invoked to explain nonspecific symptoms such as headache, irritability, muscle and joint pains, etc. (Rowe, Randolph, Rinkel)
C. 1954: "Allergic tension-fatigue syndrome" (Speer): Explained behavioral and cognitive symptoms in patients without atopic manifestation.
D. 1980's: Clinical ecology movement.
E. Related syndromes
1. Chronic fatigue syndrome
2. Closed building syndrome

III. Epidemiology

A. Prevalence is unknown
B. Risk factors (based on clinical series)
1. Females
2. Caucasians
3. Age at presentation: 20's - 40's
4. Above average SES
C. Exposure groups (from Ashford and Miller)
Industrial workersAcute & chronic exposure to industrial chemicalsPrimarily male, blue collar, aged 20-65
Tight building occupantsOff-gassing from construction materials; office equipmentor supplies; tobacco smoke; inadequate ventilationF>M; White-collar and professional workers aged 20-65 and schoolchildren
Contaminated communitiesToxic waste sites; aerial pesticide spraying; ground-water and air contamination by nearby industry and other community exposureM and F; all ages; children and infants may be affected first and/or most severely; middle-lower class
IndividualsHeterogeneous: indoor air (domestic), consumer products, drugs pesticides70-80% female; mostly in 30-50 age range; white; middle class and professional

IV. Exposures Implicated in MCS

A. Pesticides
B. Solvents and other petrochemicals
C. Formaldehyde
D. Building materials
E. Cigarette smoke
F. Perfumes and other cosmetics
G. Medications
H. Home products (cleansers, deodorizers, cooking gas)
I. Vehicular exhaust
J. Art materials

V. Pathophysiology

A. Immune dysfunction
1. Theories derive from Selye's General Adaptation Syndrome (1946). The metaphor of "total body load" is extended to the immune system following chemical exposure.
2. General focus on lymphocytes as the likely target within the immune system. Toxins are presented to lymphocytes by macrophages, especially in the setting of inflammation (which may itself be induced by environmental exposures). This both sensitizes the lymphocytes and impairs their function.
3. Organ system involvement explained by the presence of various cell types at the scene. For example, respiratory irritation leads to the recruitment of macrophages, which present immunotoxins to lymphocytes, which in turn are specifically sensitized and proliferate. But since inflamed nerve endings are present, lymphocytes are sensitized against nerve tissue as well.
4. Other theories postulate the formation of immune complexes, with environmental chemicals acting as haptens.
5. Immunologic "spreading" is postulated to account for reactivity to multiple chemicals.
6. Some writers postulate that chemical exposures trigger autoantibody formation.
7. An additional theory is that interaction of a toxin with thymic epithelial cells causes autoreactive cells to escape regulation and to proliferate.
B. Limbic/hypothalamic dysfunction
1. Neuroanatomic basis: the rhinencephalic structures
2. The relevance of kindling theory
C. Psychiatric dysfunction
1. Post-traumatic stress disorder
2. Somatoform disorder
3. Depression
4. Behavioral sensitization: symptoms viewed as a conditioned response to some stimules
5. Focus on the social environment: MCS as an exaggerated and/or irrational belief that chemicals are harming one's health.

VI. Clinical Presentation

A. General: fatigue, malaise, fevers, transient adenopathy, dry mouth, dry eyes.
B. Neurologic: Heightened olfactory sensitivity ("cacosmia"), headache, mental status changes (memory loss, absent-mindedness, difficulty concentrating, "spaciness," depression, anxiety), dizzy spells, syncope, peripheral neuropathic symptoms
C. Dermatologic: urticaria, pruritis, dry skin, tingling lips and tongue
D. Gastrointestinal: nausea, vomiting, diarrhea, constipation, anorexia
E. Genitourinary: dysmenorrhea, urinary frequency
F. Pulmonary: rhinitis, sore throat, chest tightness, wheezing
G. Musculoskeletal: arthralgias, myalgias
H. Other features of the clinical presentation (Miller)
1. Frustrating doctor-patient relationship
2. Characteristic constellation of symptoms in each patient
3. Dose dependence
4. Inter-individual variability
5. Intra-individual variability
6. Multiple exposure routes trigger symptoms
7. Subsensory triggering may occur
8. Rapid onset of symptoms following exposure
9. Variable threshold for triggering

VII. Laboratory Findings

A. Both increased and decreased complement levels have been reported
B. Increased CD4/CD8 ratio has been reported in some series, as well as increased activated T-lymphocytes (CD26)
C. Variable increases in prevalence of autoantibodies
D. No laboratory abnormalities are consistently reported

VIII. Other Diagnostic Approaches

A. Chemical and food challenges
B. Provocation-neutralization testing
C Electroencephalography

VIII. Treatment

A. General issues
1. The need for a trusting, compassionate therapeutic relationship
2. Treatment in the absence of confirmed etiologic mechanisms
3. The problem of focus on diagnosis instead of symptom management
4. Rehabilitation as the goal rather than cure
B. Clinical ecology
1. Avoidance of chemicals and certain foods
2. Rotary/elimination diets
3. Megavitamins
4. Environmental control units
5. Antifungal and/or antiviral therapy
6. Detoxification with saunas
C. Conventional medicine
1. Allergy treatment
2. Supportive care
D. Psychiatric
1. Behavioral treatment: Deconditioning through increasing exposure
2. Relaxation treatment, visualization, hypnosis
3. Pharmacologic agents: antidepressants, anxiolytics

IX. Prognosis

Further Reading:
American College of Physicians. Position paper: clinical ecology. Ann Int Med 1989; 111: 168-77.
Ashford NA, Miller CS. Chemical Exposures: Low Levels and High Stakes (New York: Van Nostrand Reinhold, 1991).
Bell IR. Clinical Ecology: A New Medical Approach to Environmental Illness (Bolinas CA: Common Knowledge Press, 1982).
Cullen MR. The worker with multiple chemical sensitivities: an overview. In: Cullen MR, Ed. Workers with Multiple Chemical Sensitivities, published as Occup Med State of the Art Rev 1987; 2: 655-61.
Hileman B. Multiple chemical sensitivity. Chem Engin News 1991; 69: 26-42.
Mitchell F (Ed.) Multiple Chemical Sensitivity: A Scientific Overview. (Princeton: Princeton Scientific Publishing Company, 1995).
Nethercott JR, Davidoff LL, Curbow B, Abbey H. Multiple chemical sensitivities syndrome: toward a working definition. Arch Environ Health 1993; 48: 19-26.
Simon GE, Katon WJ, Sparks PJ. Allergic to life: psychological factors in environmental illness. Am J Psychiatr 1990: 147: 901-06.
Smith GR, Monson RA, Ray DC. Patients with multiple unexplained symptoms: their characteristics, functional health, and health care utilization. Arch Int Med 1986; 146: 69-72.


I. Root causes

A. Population growth: The world currently has 5.7 billion people, and is projected to have about 10 billion by 2050.
B. Increasing energy use: Mostly from fossil fuels, and increasing rapidly, especially in eastern Europe and China.

II. Two related processes that result:

A. Thinning of the ozone layer
The stratosphere (20-50 km up) normally contains ozone that absorbs incident ultraviolet radiation. But chlorofluorocarbons, a family of refrigerants and aerosols, rise into the stratosphere where they undergo the following reactions:
CFC + UV radiation Cl

Cl + O3 ClO + O2

ClO + O Cl + O2

The Cl atoms are recycled, and continue attacking other ozone molecules. The thinning of the ozone layer was recognized in 1985 by the British Meteorological Survey in Antarctica, and at international meetings in 1987 and 1988, phaseout of CFCs was planned by 1999. However, the long half-life of CFCs means that current effects on the ozone layer will persist for about a century even if all production stops immediately.

B. Global warming
The greenhouse effect refers to the heat-retaining properties of the gas layer that surrounds the earth (or of the windshield in your car). Ultraviolet radiation comes from the sun, and is ordinarily reflected back from surfaces as radiant or infrared energy. The greenhouse gases retain that reflected energy. We have been increasing the amount of greenhouse gases for about 100 years.
Atmospheric Concentrations
Gas Source Pre-Industrial 1990 Change
Water vapor
CO2 Combustion 280 ppm 353 ppm 1.8 ppm/yr
CH4 Combustion peat, rice cultivation, cow flatus 800 ppb 1720 ppb 15 ppb/yr
N2O Combustion 288 ppb 310 ppb 0.8 ppb/yr
CFCs Industrial production 0300-500 ppt 10-17 ppt/yr
Ozone Automobiles

Atmospheric science is imprecise but it appears the average global temperature has increased by 0.3 to 0.6 degrees Celsius over the last century. Current estimates are that we will see a global temperature increase of 1 to 5 degrees in the next 50 to 100 years, probably in the lower end of that range. The greatest temperature increase would be in temperate zones, and the smallest increases at the equator and poles.

III. Direct and indirect effects on human health

A. From increased exposure to UV-B radiation:
1. Impaired growth of some plants (including food plants such as maize) and phytoplankton (an important component of aquatic food chains and an important fixer of atmospheric CO2).
2. Suppressed immune function.
3. Skin damage: sunburn, loss of skin elasticity, "premature aging."
4. Cancer: All skin cancers (melanomas, basal cell carcinomas, squamous cell carcinomas), lip cancer.
5. Cataracts.
B. From global warming:
1. Changed weather: more violent disturbances?
2. Changes in vegetation and food supplies: loss of some crops.
3. Further atmospheric changes: thawing of the permafrost, increased methane, causing more warming.
4. Rising sea level as polar ice caps melt: Currently estimated to reach 0.5 meters over 50 years. Loss of coastal cities and low-lying areas such as Bangladesh, Mauritius, Florida; disruption of fishing grounds; relocation of large populations.
5. Loss of drinking water supplies with salination of fresh water tables.
6. Direct effects of heat: heat exhaustion and heat stroke.
7. Infectious diseases: vector-borne diseases (malaria, eastern equine encephalitis, western equine encephalitis, St. Louis encephalitis), water-borne diseases (cholera).
8. Frightening but plausible scenarios include disruption of food supplies and famine; mass migrations; social unrest; epidemics.

IV. An imaginary look 100 years into the future: Georgia's health in 2096

Skin cancer is now Georgia's leading cancer, in both incidence and mortality. It finally surpassed lung cancer in about 2050, due to constantly increasing exposure to UV-B radiation caused by thinning of the ozone layer. The second leading cause of cancer mortality is liver cancer, although this may decrease soon. Experts attribute the pandemic of liver cancer that began in the 2040's to the chronic drought in grain-producing regions of the midwest U.S. that began a decade earlier. Because of the drought, grain from those areas became extensively contaminated by aflatoxin. But there were worldwide food shortages, and there was no choice but to consume that grain, so the FDA lifted its aflatoxin restrictions and released contaminated grain for use. However, in the last decade northern Canada and northern Russia have become the world's major suppliers of grain, and new distribution systems are in place, so it is hoped that Georgians -- indeed, all Americans -- will have uncontaminated grain to eat. Oncologists and dermatologists remain busy.

Of course, many of our health problems arise from the refugee crises of the last few decades. By 2040 the global temperature had risen an average of five degrees Fahrenheit. With melting of the polar ice caps, ocean levels had risen about one foot. Large areas of Florida and the Georgia coast became uninhabitable, both because of flooding and because of salination of the fresh water table. At the same time, the state's population had increased by 25 per cent over 1990 levels, placing great pressure on all of Georgia's fresh water. With the rising oceans, available fresh water supplies were simply overwhelmed. Truly, water is the "fluid of the 21st century," with far more social and strategic importance than oil ever had 100 years ago. It is estimated that between 2040 and 2065, 4 million people migrated into Georgia from Florida, and 3 million Georgians, mostly from coastal and southern parts of the state, became internal refugees. The metropolitan Atlanta population reached 8 million by 2060.

This helps explain the steady increase in violence as a cause of death. Violence, which 100 years ago was a leading cause of death only for selected age-sex-race groups, is now a leading cause of death for all races and both sexes, beginning at age 15. The growth of neighborhood trauma centers in the 2050's and 60's helped somewhat, but wound infections have continued to defy our efforts to treat them. It is hoped that the new 24th-generation cephalosporins will provide effective treatment for some time. Trauma surgeons remain busy, and the 18 residencies in Atlanta are expected to produce enough surgeons to meet demand through the end of the century.

Infectious disease also poses great challenges. As the global temperature continued to rise in the first few decades of the century, tropical diseases invaded Florida, and reached Georgia soon thereafter. According to the Division of Tropical Diseases at the Georgia Department of Public Health, the three leading infectious diseases in the state are now malaria, dengue fever, and yellow fever. Northern areas of the state have been relatively spared, but tuberculosis remains a serious problem in the large refugee camps in Dalton, Rome, and Gainesville. The cholera epidemics that have occurred approximately once each decade seem to be aggravated by the shortage of fresh water, which compromises sanitary practices. Bubonic plague and Lyme disease were major problems in the middle years of the century after crop failures and food scarcity displaced rodent populations from south Georgia into more populated parts of the state. However, effective rodent control campaigns in the 2060's helped control these diseases.

The heat itself is a significant cause of morbidity and mortality. Waycross now has 120 days each year with temperatures over 100 degrees, and Atlanta has 85. The mortality rate from heat stroke continues to rise slowly, especially among the elderly.

The bright spots are in the cardiovascular and respiratory diseases. Ischemic heart disease has continued to decline since the 1980's and is now rare. Experts attribute this to several factors: the virtual disappearance of smoking after 2040 when warming and water shortages caused the U.S. tobacco crop to fail, widespread caloric deprivation due to food shortages, and the general shift away from meat and dairy products due to the unavailability of grazing land. Similarly, the prevalence of asthma peaked at about 35% in 2040, and seems not to be increasing further.

Further reading:
Leaf A. Potential health effects of global climatic and environmental changes. New Eng J Med 1989; 321: 1577-83.
Longstreth J. Anticipated public health consequences of global climate change. Environ Health Persp 1991; 96: 139-44.
Last JM. Global change, ozone depletion, greenhouse warming, and public health. Ann Rev Pub Health 1993; 14: 115-36.
McMichael AJ. Planetary Overload: Global Environmental Change and the Health of the Human Species (Cambridge: Cambridge University Press, 1993).
Chivian E, McCally M, Hu H, Haines A, Eds. Critical Condition: Human Health and the Environment (Cambridge MA: MIT Press, 1993).
Health and Climate Change, a series of articles in The Lancet from October to December, 1993, and published as a monograph in 1994 (London: The Lancet, 1994).

This document was last modified on 06/14/2000 03:07:50 PM

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