Mortality among employees of lead battery plants and lead-producing plants, . Scand J Work En viron Health II (1985) 331-345. Two cohorts of male lead workers, 4 519 battery plant workers and 2 300 lead production workers, all of whom had been employed for at least one year during the period I January 1946 through 31 December 1970, were observed for mortality during the 34 years from 1 Januar y 1947 through 31 December 1980. Vital status as of the closing date was determined for 94.7 lifo of the former group and 91.6 lifo of the latter. There were 1 718 deaths in the first cohort and 621 in the second. Mortality from all causes combined was significantly greater than expected in each cohort, the standardized mortality ratio (SMR) being 107 and 113, respectively. Among the battery plant workers the greater than expected mortality rate resulted in large part from a significant number of excess deaths from malignant neoplasms (SMR 113), other hypertensive disease (mainly renal) (SMR 320), chronic nephritis (SMR 222), and a group of ill-defined conditions (SMR 355). Among the lead production workers the pattern was similar, with a significant number of excess deaths from other hypertensive disease (SMR 475), hypertensive heart disease (SMR 203), chronic nephritis (SMR 265), and ill-defined conditions (SMR 214). There was also a significant excess of deaths from external causes (SMR 143). The SMR for total malignancies was 113, but this value was not significantly elevated at the 5 % level. In neither cohort were deaths from cerebrovascular disease in significant excess, the SMR being 93 and 132, respectively. A proport ionate mortality analysis showed that the excess deaths from cerebrovascular diseaseand from hypertensive heart disease among smelter workers were in part due to the high proportion of nonwhites in the smelter populations. The stomach, liver, and lungs were the sites responsible for most excess cancer deaths in both cohorts, but the elevated SMR values were statistically significant only for gastric and lung cancers in battery plant workers. There were no excess deaths from malignancies of the kidney, brain, or Iymphopoeitic system in either cohort. It is impossible to relate the observed mortality to levels of lead exposure; because of meager quantit ative information prior to 1960. It is known that past exposures had been very high. Ethnicity, diet, alcohol, and cigarette smoking could not be ruled out as possibleconfounding etiologic factors for the cancer deaths.

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Methylcyclopentadienyl manganese tricarbonyl (MMT) is effective in raising the octane level of gasoline and is currently used in Canada for that purpose in a maximal concentration of 18 mg Mn/l (slightly less than 0.07 g Mn/U.S. gal). It has been estimated that if MMT were used in all U.S. gasoline in these amounts, the median increase of Mn in ambient air would be not more than 0.05 microgram Mn/m3, with increments generally less than 0.5 microgram Mn/m3 along urban corridors. The scientific literature was reviewed to determine how the increases in environmental manganese predicted from MMT use would relate to the amounts in the natural environment and necessary to life and to the concentrations associated with toxic effects. Even with additional manganese from the use of fuel additives, total Mn intakes would remain within the range of average amounts absorbed from food and water. Respirable manganese in ambient air due to MMT combustion would be many order of magnitude below the concentrations associated with occupational manganism and respiratory problems and also below those reported in isolated episodes of respiratory symptoms in communities near ferromanganese plants. Evidence was reviewed on the possibilities of: (1) increased absorption of inhaled manganese compared with ingested manganese; (2) hypersusceptibility of infants and persons of advanced age; and (3) increased absorption associated with iron deficiency. While relevant to high levels of exposure, these factors would not be expected to lead to toxic effects from the very low concentrations of Mn resulting from MMT use. Experimental animals that inhaled the combustion products of MMT in concentrations of approximately 10, 100, and 1000 micrograms Mn/m3 for 9 mo did not show toxic effects, although there was temporary elevation of tissue levels of Mn. Rhesus monkeys, susceptible to the neurologic effects of Mn, showed no symptoms after inhaling the combustion products of MMT in concentrations of 100 micrograms Mn/m3 for up to 66 wk. Monkeys exposed to 5000 microgram Mn/m3 also showed no symptoms. There is thus a wide margin of safety between the intakes of Mn essential to health and the high concentrations that have been associated with toxic effects. The small amounts of manganese added to the environment by the combustion of MMT used as a fuel additive would be comparable to the normal background and should not create health problems.

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