Chronic Respiratory Disease in an Industrial Town: A Nine-year Follow-up Study

Higgins, I. T. T.; Gilson, J. C.; Ferris, Benjamin G.; Waters, W. E.; Campbell, Harry; Higgins, M.

doi:10.1159/000192659

Cited by 14 publications

(14 citation statements)

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“…There is also some tendency for an increased change with age over the 10-yr period. This can also be seen in Table 7 and is similar to that reported by Fletcher et al (1976) and Higgins et al (1968) if the same group is followed over time. Some of the younger categories, as in the chlorineand S02-exposed groups, showed improvement or no change over the 10 years.…”

Section: Morbidity Studysupporting

confidence: 90%

Mortality and morbidity in a pulp and a paper mill in the United States: a ten-year follow-up.

Ferris¹,

Puleo²,

Chen³

1979

Occupational and Environmental Medicine

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Two hundred and seventy-one men seen in 1963, who worked in a pulp and a paper mill, were followed up ten years later, in 1973. Death certificates were obtained for those who died. There did not appear to be any increased mortality in the group, nor was there any increased specific cause of death. A morbidity study of 200 men seen at both times did not show any differences in respiratory symptoms or prevalence of chronic non-specific respiratory disease. Analysis of pulmonary function showed little, if any, difference between groups. Analysis of retired, deceased, and still-working categories did suggest that exposures to Cl2 or SO2 might have a slight adverse effect on pulmonary function.In 1963 we made a cross-sectional study on a group of men who had been working in a pulp and a paper mill in Berlin, New Hampshire, USA (Ferris et al., 1967). Our purpose at that time was to see whether the exposure at work had an effect on chronic non-specific respiratory disease or pulmonary function. That study showed that the workers had less chronic non-specific respiratory disease than the general population, but the older men who had been exposed to chlorine and who were cigarette smokers had slightly lower expiratory flow rates at 50, 25, and 12-5 % of vital capacity than the men who had not been exposed to chlorine.In 1973 we restudied that cohort to determine whether they had a higher mortality than expected, or had developed respiratory disease. Methods PLANT PROCESSESThe pulp mill complex contained two chemical pulp mills-one a Kraft mill and the second a sulphite mill and, in addition, a chlorine plant. The sulphite mill and chlorine vlant were phased out after 1963, and the Kraft process increased. In both mills, wood chips are introduced into large

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Section: Morbidity Studysupporting

confidence: 90%

Mortality and morbidity in a pulp and a paper mill in the United States: a ten-year follow-up.

Ferris¹,

Puleo²,

Chen³

1979

Occupational and Environmental Medicine

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“…There was no significant deviation from linearity. The decrement in the low exposure groups (-12 ml) is clearly within expected limits for normal populations while that in the high exposure groups (-205 ml) is clearly excessive (Kory et al, 1961;Ferris et al, 1965;Rosenzweig et al, 1966;Fletcher, 1967;Higgins et al, 1968;Morris et al, 1971). The five subjects who had been excluded because of mixed exposure levels were also evaluated.…”

Section: Resultsmentioning

confidence: 92%

Chronic pulmonary function loss from exposure to toluene diisocyanate

Wegman

Peters

Pagnotto³

et al. 1977

Occupational and Environmental Medicine

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In 1972 a total of 112 workers exposed to toluene diisocyanate (TDI) were examined for acute pulmonary function changes during a work shift on the first day of the working week. A dose-response relationship was demonstrated for the acute effects of TDI in this population. The cohort was restudied in 1974 to determine whether there was excessive loss of pulmonary function, and if so, whether there was an exposure level below which this did not occur. The original cohort was reduced to 63 workers available for re-survey of which 57 could be assigned reliable personal exposure levels for the two-year study period. Pulmonary function measurements were made again before and after work on the first day of the working week. A total of 132 environmental samples were collected on this and previous occasions during the study period. The 57 workers were divided into three exposure subgroups (≤ 0·0015; 0·0020 - 0·0030; ≥ 0·0035 ppm). Using the FEV1·0 as a measure of response, a dose-response relationship was observed. Only those in the lowest exposure subgroup showed normal two-year declines. The FEV1·0 of those in the highest exposure group fell 206 ml in two years (103 ml/year) which exceeds the expected value by three- to fourfold. The decrement of FEV1·0 in the middle exposure group was borderline (42 ml/year). These differences in FEV1·0 by exposure subgroup were not explained by age, months employed, smoking habits, or variables related to lung size. A significant association (r = 0·35, p < 0·005) between acute and chronic decrement in FEV1·0 was shown again. We conclude that chronic occupational exposure to TDI at 0·003 ppm or higher is unsafe.

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“…Higgins et al [13] found mean FEV 1 declines of 32 ml/year in workers aged under 34 years and 41 ml/year in workers aged 54 years and over. Fletcher and co-workers [11] found that non-smoking men under the In sub-group (n = 15) exposed to peaks of 30 ppb or above for % maximal mid-expiratory¯ow, FEV% at 25% of FVC age of 50 years had FEV 1 declines of 33 and 42 ml/year over 50 years.…”

Section: Comparison With Other Industrial Longitudinal Studiesmentioning

confidence: 98%