Abstract
Air pollution, water and soil pollution produce impaired quality of life and expose the population to contaminants that can cause cancer. One of the main pollutants are DLC, a group of highly toxic chemicals that enter the body in about 90% through our food, and are classified as type I carcinogens by the International Agency for Research on Cancer. In the U.S. and Europe during the twentieth century there was an increase in the incidence of NHL that has stabilized in recent years which is coincident with the implementation of strong dioxin emission regulations.
In Chile there has been a higher incidence of NHL in recent decades so we decided to evaluate DLC levels in patients with NHL and compared them with a normal control population.
In order to achieve this goal a descriptive observational, case-control unpaired, epidemiological study was designed. Patients with NHL diagnosed in the Hospital of Valdivia in 2011 and 2012 were considered in the study. The control group was composed by individuals without cancer, from the same geographical area as the patients. All volunteers were asked if they wished to participate in the study using an informed consent. Blood sample without anticoagulant was obtained from each individual. Serum was aliquoted and stored at -20 ° C for later quantification of total lipids and DLC with sulfo-phospho-vanillin assay colorimetric method and DR-CALUX ® Bioassay, respectively (screening method approved by FDA and EEC). A nonparametric statistical hypothesis was constructed using Wilcoxon rank sum test to compare two independent samples considering a non-symmetrical distribution of the variable DLC (pg TEQ / total lipids) and a significance level of α= 5%.
51 patients with NHL and 100 controls entered the study. The mean ages of the LNH group and the control group were 59±14.5 and 39± 16.9 years, respectively. The male/female ratio was 0.52 and 0.82 in the LNH and control group, respectively. NHL cases were from southern regions of Chile matching that of controls in a 100%. The histopathology of NHL cases was in 90% of B lineage. The concentration of DLC was quantified in all cases and expressed in toxicity equivalents (TEQ) using as reference the 2,3,7,8, tetracloroparadibenzodioxine and corrected to the value of total serum lipids (pg TEQ / total lipids). In all samples analyzed DLC were detected. The DLC levels found for NHL cases and controls were 28.33 ± 28.57 and 15.02 ± 7.64 pg TEQ / total lipids, respectively. The median values for cases and controls were 19.02 and 12.67 pg TEQ / total lipids, respectively. The analysis with Wilcoxon rank sum test showed a statistically significant evidence (z = -4.44, p = 0.0000) (Figure 1).
Box plots showing dioxin concentration on a serum lipid basis.
The cases and controls analyzed came from a geographical area of 1200 km of extension without polluting industries having detectable levels of DLC in all them. DLC levels NHL cases were higher compared with controls.
When comparing the results of the controls (15.02 pg TEQ / g lipid) with other studies in unexposed populations we find similar levels in Northern Australia and Taiwan, 10.9 and 15.2 pg TEQ / g lipid, respectively (Harden et al. 2007 and Chen et al., 2005). Levels are higher in areas with higher industrial activity as France, Slovakia and Belgium (Marchand et al. 2004 Chovancová et al 2012, Bilau et al., 2009), and lower for residents of Fukuoka and Athens (Masuda et al. , 2005 Costopoulou et al., 2006). The vast region from which the controls come from in our study, with an environment relatively free of pollution leads us to infer that DLC are basically food contaminants, since the majority of the population consume food products manufactured in areas of high industrial activity and distributed throughout the country.
DLC studies in populations exposed to higher pollution (Viel et al., 2008) have shown increased incidence of NHL in those areas. This makes us pose the hypothesis of a potential pathogenic role of DLC in NHL that could be mediated by genetic mechanisms and / or deregulated B cell expansion.
This research is funded by FONIS SA11I2029 (National Fund for Health Research).
No relevant conflicts of interest to declare.
