Evidence for the effect ofoccupational exposure to lead on the male endocrine system is conflicting. This study evaluated the primary (testicular) and secondary (hypothalamo pituitary testicular) effects of exposure to lead in 122 current lead workers and 49 non-exposed workers. The mean current blood lead concentration was 35-2 (range 9-6-77-4) pg/dl in the exposed workers, and 8-3 (range 2-6-14-8) pg/dl in the non-exposed workers. Concentrations of plasma luteinising hormone (LH) and follicle stimulating hormone (FSH) were both significantly higher in the exposed workers, but testosterone (T) was not significantly different between the two groups. In older exposed workers, however (> 40 years), plasma T concentrations were significantly lower, but LH and FSH concentrations were not significantly different. Compared with non-exposed workers, those exposed for less than 10 years had significantly raised LH and FSH and normal T concentrations whereas those exposed for 10 or more years had significaaitly lower T, and normal LH and FSH concentrations. More recently, studies of lead exposed workers have reported positive evidence of a central effectthat is, a disruption of gonadotrophin secretions. Progressive increase in plasma LH and decrease in plasma T concentrations with no change in FSH was noted among workers exposed to a mean blood lead concentration of 70 ,ug/dl for less than one year (five subjects), one to five years (eight subjects), and more than five years (11 subjects) compared with controls (20 subjects).9 On the other hand, Gustafson et al recently reported lower plasma FSH and LH concentrations (especially in workers less than 40 years of age) and no difference in T concentrations in 25 workers compared with age matched controls.'0 The levels of lead absorption were moderate (mean blood lead 40 ,ug/dl, mean duration (SD) 6-4 (4-1) years). The results in some studies were difficult to interpret for reasons such as small sample sizes, possible confounding effects by age and other factors, and on 7 June 2019 by guest. Protected by copyright.

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Ventilatory function and airway reactivity of 20 firefighters were studied one hour before and one hour after exposure in a smoke chamber. None showed an increase in airway reactivity to inhaled histamine before exposure. Eight (80%) of the regular firefighters, however, had an increase in airway reactivity after exposure in the smoke chamber. After six hours, three of the firefighters still had increased airway reactivity. All were nonreactive after 24 The HCT was performed using standard concentrations of histamine diphosphate solution delivered by a hand held De Vibliss No 40 glass nebuliser. The mouthpiece of the nebuliser was placed between the teeth of the subject who exhaled to slightly below functional residual capacity (FRC) and then inhaled slowly over one to two seconds towards total lung capacity (TLC), at which stage he was required to hold his breath for three seconds. At the beginning of inspiration the operator gave the bulb of the nebuliser one firm squeeze. The FEV1 was measured 60 seconds after each dose and followed immediately by the next dose. The challenge was stopped when the FEV, fell by more than 20% from the postsaline value or when the maximum dose of 3 9 umol was 524 on 27 April 2019 by guest. Protected by copyright.

Urinary N-acetyl-/I-D-glucosaminidase (NAG) had been shown to be a useful early marker of renal injury. In workers exposed to lead it seems to be the only early marker but the dose response and dose effect relations are weak. Furthermore, the significance and underlying mechanism of increased urinary NAG activity is far from clear. By studying the isoenzyme profiles of urinary NAG, the significance and underlying mechanism may be further clarified. The heat labile (NAG-A) and heat stable (NAG-B) isoenzyme profiles of 128 workers exposed to lead from a lead stabiliser factory were analysed. NAG activity was expressed as total NAG, NAG-A, and NAG-B activity as well as ratios (NAG-B/total NAG and NAG-B/NAG-A). Exposure indices included the recent concentration of blood lead (BPb), a cumulative blood lead index (TBPb), and the recent change in concentration of blood lead (CBPb). The NAG indices correlated best with CBPb. Nearly 50% of the variation in NAG-B activity could be explained by the combination of all three exposure indices but only the CBPb was highly significant. When these exposure indices were entered separately into the regression equation, CBPb accounted for 36-3% of the variation in NAG-B activity, 5-7% was accounted for by TBPb and 2-7% by BPb. There was also no dose-effect or dose-response relation between the NAG variables and BPb or TBPb groups. With CBPb, there were dose-effect and doseresponse relations. With CBPb, there was an increase in NAG variables in the group with more than 25% increase in blood lead over the past six months. The increase in NAG activity in this study is likely to be due to a recent increase in concentration of blood lead and hence presumably a recent rise in renal burden of inorganic lead. This suggests that the increase in urinary NAG activity is a form of acute response to a sharp increase in renal burden of lead, rather than to a cumulative dose. Heat stable NAG is part of the lysosomal membrane and is present in the urine when there is breakdown of lysosomes. Our data therefore contradict suggestions that the increase in urinary NAG activity is due to exocytosis.(Occup Environ Med 1994;5l:125-129)

Cadmium induced renal tubular effects were examined in 65 female workers in a factory manufacturing nickel cadmium batteries. Urinary #2-microglobulin (fi2m), urinary N-acetyl-Dglucosaminidase activity (NAG), and serum creatinine and serum urea concentrations were used to assess the renal effects. Of the four measures, only urinary NAG and urinary fl2m showed a strong positive correlation with blood cadmium concentrations (r = 0-49 and 0-43 respectively); NAG showed a weaker correlation with urinary cadmium concentrations (r = 0-35). Urinary fi2m has weak correlation with urinary cadmium (r = 0 04). Only urinary NAG showed a significant deterioration in renal function among the exposed group. NAG detects the largest proportion of abnormalities among the exposed group. Abnormal urinary ,B2m is detected in only 15 4% of the workers, half of whom have blood cadmium above 10 ug/l. The proportion of abnormalities detected by urinary NAG differs significantly from the proportion of abnormalities detected by urinary f,2m (p < 0-01).The age adjusted mean urinary NAG excretion showed a significant rise with urinary cadmium of above 3 ,ug/g creatinine. Urinary ,B2m failed to show any significant rise. With blood cadmium concentrations, the age adjusted mean urinary NAG excretion showed a rise from 1 jg/l of blood cadmium followed by a plateau between blood cadmium concentrations of 3-10 jg/l. No significant rise in mean urinary excretion in f2m was seen until blood cadmium concentrations exceeded 10 pg/l.