Case Studies in Environmental Medicine: Environmental Triggers of Asthma

The case studies series is a key part of the agency's health professional environmental education strategy. The case studies are available free of charge to educate health professionals about hazardous substances. The case studies are accredited and offer continuing education credits for doctors and nurses. A brief introduction to the case study follows.

Case Study

A 12-year-old girl arrives at your office with her mother for an evaluation of her cough. The mother reports that her daughter has had a nocturnal nonproductive cough two to three times per month for the past 3 months associated with increasing episodes of shortness of breath that resolve spontaneously. During soccer games, the girl has recurrent episodes, which are only relieved when she uses a friend's albuterol inhaler.

Past medical history reveals that the patient has had recurrent upper respiratory infections and had bronchitis 2 years ago. The patient has had no hospitalizations or emergency department visits.

Current medications include diphenhydramine for her intermittent runny nose and an occasional puff from her friend's inhaler during soccer games.

Family history reveals that the girl lives with her mother, father, and older sister in a house on the outskirts of the community. The father had a history of seasonal hay fever as a child. Both parents are smokers, and the mother reports that her husband has had some difficulties with episodic cough and shortness of breath, but has not seen a physician.

For nearly two decades, scientists have been concerned about the potentially serious effects of several categories of chemicals in the human endocrine system. Endocrine disruptors are thought to

• mimic natural body hormones;
  
  
• inhibit the actions of natural body hormones; or
  
  
• alter the normal regulatory function of the immune, nervous, and endocrine systems (1).

Many persistent organic chemicals have been implicated in endocrine disruption including pesticides, dioxin, polychlorinated biphenyls (PCBs), and DDT. Much of the evidence for endocrine disruption is gleaned from observations in birds, fish, and wildlife. Some adverse health effects include

• abnormal thyroid function and development in fish and birds;
  
  
• decreased fertility in shellfish, fish, birds, and mammals;
  
  
• decreased survival of offspring; and
  
  
• alteration of the immune and behavioral function in birds and mammals (1).

Many suspected endocrine-disrupting chemicals are environmentally persistent and lipophilic. The effects of mixtures of chemicals that might affect endocrine function must also be considered. Finally, and perhaps most importantly, we must consider the fact that susceptible populations, such as young children and persons who live near hazardous waste sites and who might be exposed via contaminated soil and water, might be at greater risk for adverse health effects of endocrine-disrupting chemicals. Results of research from the Agency for Toxic Substances and Disease Registry's (ATSDR) Great Lakes Human Health Effects Research Program have demonstrated elevated exposures and intrinsic physiologic susceptibility in sensitive populations such as subsistence anglers, American Indians, pregnant women, young children, men and women of reproductive age, the elderly, and the urban poor (2).

Scientists continue to debate various issues surrounding endocrine disruption, including the name itself (see sidebar article). To fully assess the public health implications of endocrine disruption, many unanswered questions must be addressed. A report by the National Research Council (NRC) Committee on Hormonally Active Agents in the Environment evaluated mechanisms of action, health effects, exposure, dosimetry, and screening and monitoring (3). The committee made several recommendations including the following:

• Further research to better elucidate underlying mechanisms of action of hormonally active agents.
  
  
• Continued monitoring for abnormal development and reproduction in wildlife and human populations.
  
  
• Longitudinal tests of developmental milestones from conception through adulthood and a standardized test to study neurobiologic and social development.
  
  
• Studies of the prevalence of autoimmune problems.
  
  
• Studies of possible associations between exposure and various cancers, including the development of animal models.
  
  
• Long-term studies of exposed populations.
  
  
• Better monitoring of contaminated media to determine environmental concentrations, as well as background concentrations of hormonally active agents in humans.

Addressing the committee recommendations will enable scientists to obtain a clearer picture of the human health and ecologic effects of endocrine-disrupting chemicals and allow appropriate public health policies to be set. Both the EPA Endocrine Disruptor Screening and Testing Advisory Committee report (4) and the NRC (3) committee report recommended that chemicals be screened and monitored for endocrine-disrupting potential. Following the recommendations of its committee, EPA implemented a screening and testing program that will determine what, if any, endocrine-mediated adverse effects occur as a result of exposure to chemicals. ATSDR included endocrine disruption as a part of one of its focus areas in the agency's Agenda for Public Health Environmental Research [APHER] 2002-2010 (5). APHER includes several areas of concern that, like endocrine disruption, have critical data and information gaps. Research results will be used to improve ATSDR's public health activities and interventions for communities exposed to hazardous waste substances through contaminated water, soil, air, or food (5).

References

1. Crisp TM, Clegg ED, Cooper RL, Wood WP, Anderson DG, Baetcke KP, et al. 1998. Environmental endocrine disruption: an effects assessment and analysis. Environ Health Perspect 1999;106 (suppl 1):11-56.

2. Hicks HE, Cibulas W, De Rosa C. The impact of environmental epidemiology/toxicology and public health practice in the Great Lakes. Environ Epidemiol Toxicol 2000;2:8-12.

3. Committee on Hormonally Active Agents in the Environment, National Research Council. Hormonally active agents in the environment. Washington (DC): National Academy Press; 1999. p. 1-9.

4. US Environmental Protection Agency. 1998. Endocrine Disruptor Screening and Testing Advisory Committee (EDSTAC) final report. Washington (DC): US Environmental Protection Agency. Available from URL: www.epa.gov/scipoly/oscpendo/history/finalrpt.htm .

5. Agency for Toxic Substances and Disease Registry. Agenda for public health environmental research (APHER), Agency for Toxic Substances and Disease Registry, 2002-2010. Atlanta: US Department of Health and Human Services; 2001.

[Table of Contents]

Chronology of Terminology

With the exception of the naturally occurring ore, beryl, all compounds of the metal beryllium are potentially harmful, particularly if inhaled. Soluble beryllium compounds produce both acute and chronic toxicity. Insoluble forms, such as beryllium alloys, intermetallics, beryllium oxide, and beryllium ores, generally induce effects only after prolonged exposures.

Beryllium and its compounds can be highly toxic, and exposure can lead to adverse health effects. The metal can be absorbed through the lungs or the skin, particularly if the skin is not whole. In contrast, beryllium usually is not hazardous if ingested (1,2). Beryllium exposure might have local effects; however, the systemic changes are usually more significant. Once absorbed through the lungs or skin, beryllium can be deposited in the spleen, liver, and bones (1). The rate of excretion of beryllium in the urine depends on how rapidly and in what form the metal has been absorbed. Beryllium can persist in the liver and bones after it has been excreted by the lung.

Most acute health effects result from relatively high exposuresometimes from only a one-time exposure. Most chronic health effects result from repeated exposures, sometimes at levels not high enough to make a person immediately sick.

Beryllium can be tested in the urine; however, beryllium in the urine only indicates that exposure has occurred: the level does not correlate with severity of exposure or clinical findings (2). Specific tests for beryllium in lung and skin tissue are also available (2). Other types of lung disease, particularly sarcoidosis, must be ruled out. The skin can also be affected by chronic beryllium exposure (1). Contact with the broken skin can cause itchy ulcers and lumps or nodules to develop on the exposed part of the body after an incubation period of about 2 weeks. Accidental implantation of beryllium metal in the skin might produce a "beryllium ulcer" or granuloma. These ulcers can be chronic.

Treatment of chronic beryllium disease, or berylliosis, is dependent on severity of the symptoms, and should include removing the person from exposure. Corticosteroids can be a useful adjunct for controlling symptoms of shortness of breath and for delaying onset of heart failure (2). Chronic skin granulomas can be surgically removed.

Whether beryllium compounds are carcinogenic in humans remains controversial (2). Some evidence shows that beryllium causes lung cancer in humans, and beryllium has been shown to cause lung and bone cancer in experimental animals (2,3). Insufficient information is available to classify beryllium as a reproductive hazard (2). Individual sensitization and hypersensitivity reactions to beryllium compounds, particularly beryllium fluoride, beryllium chloride, and sulfate, also occur with exposure (1,2).

Conclusion

Medical tests that look for damage already caused are not a substitute for controlling exposure. All unnecessary beryllium exposure must be avoided. Unless a less toxic chemical can be substituted for beryllium, engineering controls are the most effective way of reducing beryllium exposure. Because dust control is of paramount importance, the best protection is to enclose operations and provide local exhaust ventilation at the site of chemical release. Wet, self-contained processes should be used. Beryllium preparations should be transported as liquids rather than powders. Respirators, masks, protective eyewear, clothing, and gloves are less effective than the controls already mentioned, but are sometimes necessary to prevent exposure. Even with optimal care, the concentration of beryllium in the air might be sufficient to induce hypersensitivity in some individuals (1). The Occupational Safety and Health Administration, which adopts and enforces health and safety standards, requires employers to determine the appropriate personal protective equipment for each hazard, including exposure to beryllium and beryllium compounds, and to train employees on how and when to use protective equipment.

References

1. Morgan WK, Seaton A. Occupational lung disease. 2nd ed. Philadelphia: W.B. Saunders Company; 1984. p. 458-68.

2. MEDITEXT medical management: beryllium compounds. In: Heitland G, Hurlbut KM, editors. TOMES system. Englewood (CO): Micromedex; 1998 Dec.

3. New Jersey Department of Health and Senior Services. Beryllium: hazardous substance fact sheet. Trenton (NJ): New Jersey Department of Health and Senior Services; 1998.

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This page last updated on October 28, 2003
Contact Name: Wilma López/ WLópez@cdc.gov