A susceptible population will exhibit a different or enhanced response to HCCPD than will most persons exposed to the same level of HCCPD in the environment. Reasons may include genetic makeup, age, health and nutritional status, and exposure to other toxic substances (e.g., cigarette smoke). These parameters may result in reduced detoxification or excretion of HCCPD, or compromised function of target organs affected by HCCPD. Populations who are at greater risk due to their unusually high exposure to HCCPD are discussed in Section 5.6, Populations With Potentially High Exposure.
People with preexisting lung, kidney, or liver damage may be more at risk than the general population in the event of HCCPD exposure because of compromised organ function. Asthmatics are probably also likely to be more affected. In two studies of human exposure to HCCPD in the workplace, respiratory symptoms predominated (Kominsky et al. 1980; Morse et al. 1979). There was also transient elevation of serum enzyme levels (e.g., LDH, AST, ASL, and AP) and proteinuria, suggesting potential effects of HCCPD on the liver and kidneys (Morse et al. 1979). Animal studies have confirmed the potential respiratory, renal, and hepatic toxicity of HCCPD. Animal studies also suggest that males are generally more susceptible to HCCPD toxicity than females (Abdo et al. 1984; NTP 1994; Rand et al. 1982a).
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.