Multivariate analysis indicated that age was the primary predictor, and noise and ultrasound exposure the secondary predictors of hearing thresholds in the high-frequency range. The results suggest that HFA could be useful in the early diagnosis of noise-induced hearing loss in younger groups of workers (under 30 years of age).

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"Would you tell me please, which way I ought to go from here," asked Alice. "That depends a good deal on where you want to go to," said the cat. (Lewis Carroll, Alice's Adventures in Wonderland) A large number of epidemiological studies show positive correlations between increasing levels of particulate matter (PM) in urban air and short-term morbidity and mortality for diverse acute cardiopulmonary diseases. Brought about by PM increments, inflammation is thought to exacerbate preexisting inflammatory diseases. Experimental evidence suggests a hierarchical oxidative stress model, in which a weakened antioxidant defense, as observed in disease or induced by inhaled particles, increases the PM ability to cause lung inflammation, accounting for exacerbations that occur in asthmatics and in patients with chronic obstructive lung disease. The role of PM-induced inflammation leading to acute cardiovascular events such as arrhythmia, heart failure, and myocardial infarction is more speculative. There is neither clear-cut evidence in humans that inhaled PM could get as far as blood circulation nor that proinflammatory mediators are significantly released from inflamed lung tissues, nor that blood coagulability is critically altered. As a whole, data in humans indicate that short-term inflammatory responses to PM are not always detected; they are usually mild and loosely correlated with functional changes. Among these studies, the diversity of PM characteristics, dose metrics, and endpoints hampers a clear discerning of inflammatory mechanism(s). Thus, the question arises as to whether inflammation represents the mechanism of acute cardiopulmonary PM toxicities in susceptible individuals, or rather an event that may coexist with other relevant mechanism(s). This review article discusses the evidence in humans linking short-term PM increments to inflammation and to exacerbations of cardiopulmonary diseases. Although there is a large amount of data available, there still remains a gulf between the number of epidemiological and panel studies and that of controlled exposures. Research on controlled exposure needs expanding, so that the results of time-series and panel studies will be better understood and short-term standards for human exposure may be more confidently allocated.

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Our study shows that exposure to ultrafine particles is associated with autonomic dysregulation in selected patients with myocardial infarction. More severe arrhythmias occur at the highest exposures to larger particles. Nevertheless, the underlying mechanisms remain hypothetical because inflammation may be evoked by PM or be related to the disease itself.

Chlorpyrifos [0,0-diethyl 0-(3,5,6-trichloro-pyridyl) phosphorothioate] caused delayed polyneuropathy in man. Contrary to previous studies, we report here that it also causes delayed polyneuropathy in the hen, the animal model for this toxicity. The minimal neuropathic dose was 60-90 mg/kg p.o., corresponding to 4-6 times the estimated LD50. Consequently, pralidoxime (2-PAM) in conjunction with atropine was necessary to reverse acetylcholinesterase (AChE) inhibition and cholinergic toxicity in hens given high enough doses of chlorpyrifos to cause neuropathy. Chlorpyrifos was slowly absorbed after single oral doses and the threshold of inhibition (greater than 70%) of neuropathy target esterase (NTE), the putative target for delayed neuropathy, was reached within 5-6 days. High AChE inhibition (greater than 90%), however, was measured within hours after dosing because of the higher potency of chlorpyrifos to inhibit this enzyme. In vitro studies showed that chlorpyrifos-oxon, the active metabolite of chlorpyrifos, was 10-20 times more active against AChE than against NTE, confirming the clinical observation. No differences were seen between human and hen enzymes in this respect. Hen and human brain homogenates contain A-esterases which hydrolysed chlorpyrifos to about the same extent in both species. In conclusion, chlorpyrifos causes delayed polyneuropathy in the hen, as was reported in man. The reasons for previous negative data in the hen are probably due to the relatively lower doses which were used. Judging from in vitro studies with hen and human enzymes, there are no differences in the two species as far as their relative sensitivity to delayed polyneuropathy. It is likely that delayed polyneuropathy would develop in both species only after severe cholinergic toxicity requiring aggressive antidotal treatment.

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