Jonathan M. Ramlow

Have sperm counts been reduced 50 percent in 50 years ? A statistical model revisited

OBJECTIVE To reanalyze data that were used in a linear model to predict that mean sperm counts have been reduced globally by approximately 50% in the last 50 years. DESIGN The mean sperm counts and their temporal distribution were reanalyzed via several different statistical models (quadratic, spline fit, and stairstep). CONCLUSION There are several reasons why a published linear regression model is inappropriate to infer a 50% reduction in mean sperm counts in the last 50 years. These include [1] the potential selection biases that may have occurred with the 61 assembled studies such that they are not representative of their underlying populations; [2] the likely variability in collection methods, in particular, the lack of adherence to a minimum prescribed abstinence period, as has been stated for the largest study, which contained 29.7% of all the subjects included in the analysis; [3] the paucity of data in the first 30 years of the 50-year trend analysis; [4] the fact that if the last 20 years of data are examined, which contains 78.7% of all the studies and 88.1% of the total number of subjects, there is no decrease in sperm counts, in fact, sperm counts were observed to have increased; [5] the conflicting data from a large individual laboratory, which was not prone to the collection variability that likely occurred between the 61 studies, that did not suggest a decline in mean sperm count or seminal volume during a comparable time period, even though this laboratory published the data that were largely responsible for the high historical values in the linear model; and, most importantly, [6] the variety of other mathematical models that perform statistically better at describing the recent data than the linear model and thus offer substantially different hypotheses. The data are only robust during the last 20 years of the analysis, in which all the models, except the linear model, suggest constant or slightly increasing sperm counts.

Mortality in a cohort of pentachlorophenol manufacturing workers, 1940-1989.

Mortality in a cohort of 770 workers with potential pentachlorophenol (PCP) exposure was evaluated from 1940 through 1989. The study cohort is a subset of a larger cohort of workers with potential exposure to higher chlorinated dioxins. Total mortality and cancer mortality in the PCP cohort were slightly lower than expected in comparison to the U.S. white male population. There were 229 total deaths with 242.5 expected (SMR = 94, 95% confidence interval 83-108), and 50 cancer deaths with 52.6 expected (SMR = 95, 95% confidence interval 71-125). In comparison with unexposed employees, the risk ratio for total mortality was 1.03 (95% confidence interval 0.90-1.17), and the risk ratio for all cancer mortality was 0.95 (95% confidence interval 0.71-1.26). In most cause of death categories of a priori interest no deaths were observed in the cohort. A small excess of other and unspecified lymphopoietic cancer deaths was observed but did not appear to be related to exposure. Excesses of deaths due to cancer of the kidney, gastric and duodenal ulcer, cirrhosis of the liver, and all accidents were observed in comparison with the U.S. white male population and with unexposed employees. These were associated with increasing estimated cumulative PCP exposure after lagging exposures by 5 and 15 years. Despite the limited size and the generally favorable total mortality experience of the cohort, it was concluded that cohort members may have incurred increased risk of death due to some specific causes. The risks could not, however, be attributed conclusively to PCP exposure and may have been associated with other occupational and nonoccupational factors. Additional mortality surveillance of this cohort will be performed.

Mortality from pancreatic and lymphopoietic cancer among workers in ethylene and propylene chlorohydrin production

OBJECTIVES: A previous study reported a fivefold increase in mortality from pancreatic cancer and a threefold increase in lymphopoietic and haematopoietic cancer among 278 men who were assigned to a now dismantled Union Carbide chlorohydrin unit in the Kanawha Valley of West Virginia. There were also significant trends with duration of employment. The purpose of this study was to determine whether a comparable increased risk in mortality from pancreatic cancer and lymphopoietic and haematopoietic cancer occurred among male employees assigned to the Dow Chemical Companys ethylene and propylene chlorohydrin production processes. METHODS: The cohort consisted of 1361 male employees who worked at the companys Freeport, Texas, Plaquemine, Louisiana or Midland, Michigan plants. Subjects were considered to have had a minimum of 30 days of workplace experience in 1940-92, in the ethylene chlorohydrin and propylene chlorohydrin process areas. These process areas were located within the ethylene oxide and propylene oxide production plants. A total of 300 deaths was observed to 31 December 1992. RESULTS: The standardised mortality ratio (SMR) for all malignant neoplasms was 94 (95% CI 74 to 118). There was one pancreatic cancer death compared with 4.0 expected (SMR 25, 95% CI 1 to 140). There were 10 lymphopoietic and haematopoietic cancer deaths compared with 7.7 expected (SMR 129, 95% CI 62 to 238). Additional analyses, which examined location, production process, duration of employment, and a 25 year induction latency period, were not significant. CONCLUSIONS: The results provide some assurance that the Dow Chemical cohort, to date, has not experienced increased risks of pancreatic cancer and lymphopoietic and haematopoietic cancer as previously reported in a different cohort of chlorohydrin workers. Possible reasons are discussed for the inconsistent findings between the two cohorts.