Hair Dye Use and Other Risk Factors for Leukemia and Pre-leukemia: A Case-Control Study

Abstract

A case-control study was carried out to examine the relation of three subtypes of leukemia cells and refractory anemia with excess of blasts to selected behavioral and environmental factors. Cases aged 15 years or older were recruited in three hospitals located in Rome, Bologna, and Pavia, respectively. Outpatients who were either normal or had nonneoplastic hematologic disorders and were seen in the same hospitals as the cases were enrolled as controls. Two hundred fifty-two patients with acute myeloid leukemia, 100 with acute lymphocytic leukemia, 111 with refractory anemia with excess of blasts, 156 with chronic myeloid leukemia, and 1,161 controls were included in the study. Refractory anemia with excess of blasts and chronic myeloid leukemia were included because they are regarded as forms of pre-leukemia. Odds ratio estimates were generally imprecise, but associations were suggested between specific case subtypes and exposure to dark hair dye, selected occupations (shoemaker, painter, electrician, child care), residence in houses built with tuff, and smoking. Although the exploratory nature of the study and its limited statistical power preclude firm conclusions, its results are consistent with those of previous studies, and are in general biologically plausible.

Tobacco and the risk of acute leukaemia in adults

“…Evidence that current smokers have increased risk of acute leukaemia has been found in three other case-control studies (Severson et al, 1990;Brown et al, 1992a;Mele et al, 1994). Tests for trend in number of years since stopped uses 21+ years as baseline; χ 2 = 0.54 (P = 0.76) for acute leukaemia, χ 2 = 1.64 (P = 0.44) for AML, and χ 2 = 0.79 (P = 0.68) for ALL.…”

“…More consistent with this study were the relatively constant odds ratios for AML with years smoked observed in another study (Brown et al, 1992a). Although significant increasing trends of pack-years were reported in previous studies (Severson et al, 1990;Sandler et al, 1993;Mele et al, 1994), it was felt that for the current analysis pack-years were inappropriate as not only does this variable not account for time with respect to diagnosis, it also accrues errors resulting from recall bias. Moreover, the presented results suggest that those who stopped smoking over 20 years before diagnosis were not at risk and so an analysis of lifetime exposure expressed in pack-years is probably unsuitable.…”

“…While published evidence for leukaemia and self-reported tobacco use is inconclusive (Kinlen and Rogot, 1988;Brownson, 1989;McLaughlin, 1989;Garfinkel and Boffetta, 1990;Mills et al, 1990;Spitz et al, 1990;Brownson et al, 1991;Linet et al, 1991;Brown et al, 1992a;Sandler et al, 1993;McLaughlin et al, 1995;Engeland et al, 1996;Adami et al, 1998), studies tend to suggest a weak association for AML (Severson, 1987;Brownson, 1989;Severson et al, 1990;Brownson et al, 1991;Brown et al, 1992a;Friedman, 1993;Sandler et al, 1993;Mele et al, 1994;Pasqualetti et al, 1997), with only a few studies not reporting an increased risk (Cartwright et al, 1988;Kabat et al, 1988;Spitz et al, 1990;Crane et al, 1992). Indeed, pooling the odds ratios from all case-control studies published to date suggests that smoking could increase the risk of AML by about 20% (Table 3).…”

“…Interestingly, the pooled risk estimate changes little when only population-based case-control studies (Severson, 1987;Severson et al, 1990;Brown et al, 1992a;Sandler et al, 1993; and the present study) are considered, despite there being less evidence of heterogeneity (χ 2 = 4.99, P = 0.29). Published evidence does not favour an association between ALL and smoking (Kabat et al, 1988;Brown et al, 1992a;Sandler et al, 1993;Mele et al, 1994;Pasqualetti et al, 1997), possibly as many studies lack power to detect a significant risk due to small numbers of cases. Indeed, only one case-control study of comparable size to the present has been published, with a risk estimate and 95% confidence interval (OR = 1.3, 95% CI 0.8-2.0) similar to the result reported here (Sandler et al, 1993).…”

“…This suggests that the increased risk from smoking for ALL may be similar to that for AML. Dose-response relationships for AML and ALL have previously been evaluated using the number of cigarettes consumed per day (Kabat et al, 1988;Brownson, 1989;Severson et al, 1990;Brownson et al, 1991;Brown et al, 1992a;Crane et al, 1992;Friedman, 1993), the number of years smoked (Severson, 1987;Severson et al, 1990;Brown et al, 1992a;Friedman, 1993), or pack-years (Severson et al, 1990;Crane et al, 1992;Sandler et al, 1993;Mele et al, 1994). While the majority of studies found no evidence of a trend in risk with number of cigarettes smoked per day (Kabat et al, 1988;Brownson, 1989;Brownson et al, 1991;Brown et al, 1992a;Crane et al, 1992), significant increasing trends with increasing number of years smoked were found in two studies (Severson, 1987;Severson et al, 1990).…”