Minor sources (inhalation) of chromium may be road and cement dust, erosion products of brake linings and emissions from automotive catalytic converters, and tobacco smoke. Cigarettes contain 0.24 to 14.6 mg/kg chromium, although it is not known how much of this is inhaled. Foodstuffs (ingestion) generally contain extremely low chromium levels.
If effluent from the plant has reached the groundwater, community residents who drink well water may be at risk. Airborne plant emissions may have also reached nearby residents. Workers at the plant who prepare the plating baths and work near them may be receiving significant exposure.
Chromium (VI) is a powerful oxidizing agent. In the plasma and cells, it is readily reduced to chromium (III), which is excreted in the urine.
Yes, persistent dermal ulcers, respiratory tract irritation, and pulmonary sensitization are all possible effects of chromium exposure.
While it cannot be ruled out, it is unlikely that the dermal and inhalation chromium exposure of this patient will cause lung cancer. Persons who have developed lung cancer after chromium exposure were workers who had significant inhalation exposure for 2 years or longer. Because this patient’s inhalation exposure is at ambient air levels and probably of 2 years duration at most, any increase in his relative risk would not be great. The patient should be advised to stop smoking cigarettes because smoking may act synergistically to increase risk and is itself a significant risk factor for lung cancer. The data is insufficient to estimate the risk from ingestion of the contaminated drinking water.
If exposure was recent, chromium levels in blood or urine may be used to confirm exposure. Renal function should be tested (urinalysis, BUN, creatinine, and ß2-microglobulin) to determine if renal tubular damage has occurred.
No useful interpretations can be drawn from the hair analysis. A result of 1038 ppm is beyond the range for unexposed persons (50 to 1000 ppm); however, the sample could have been environmentally contaminated with chromium from the water during bathing, or by chromium in ambient air polluted by the plant emissions. There are no standard methods for obtaining a hair sample nor for washing and preparing it for analysis, and these techniques can greatly influence results. Finally, there is no research that proves a correlation between chromium content of hair and exposure levels or physiologic effects; therefore, the result has no clinical significance.
If the sources of chromium exposure can be eliminated for this patient, except for the skin lesions, no further treatment would be required. Topical ascorbic acid has been useful in the treatment of chrome ulcers and 1% aluminum acetate wet dressings can be used to treat the dermatitis.
This patient’s case may be a sentinel for community exposure. You should contact the local health department, OSHA, and EPA to report your patient’s adverse effects and discuss your suspicions of the chromium source. Chromium levels in and around the plant should be measured. If a hazard exists, workers should be provided proper protective gear, trained, and medically monitored. Since EPA does not currently have an emission standard, it may be difficult to abate the atmospheric source of chromium. Decontamination of the pond site may require regulatory action and litigation. Residents who use well water should be encouraged to use an alternate water source for drinking and cooking.