sample was above the 25th percentile of meas- ured concentrations, they were assigned to a separate exposure group (modeled as a dummy variable). For linear analyses (of continuous exposures), the concentration for subjects with sample LODs below the 25th percentile was imputed as the specific LOD for the sample, whereas those with sample LODs above the 25th percentile were included in a separate exposure group, as above. This strategy assumes no (categorical analyses) or low (linear analyses) exposure misclassification. Analyses were conducted for individual organochlorines, as well as for the sum of PCB congeners, chlordanes (cis- and trans-nona- chlor and the metabolite oxychlordane), and DDTs (DDT and DDE). In one of the analy- ses, we grouped PCBs according to immuno- toxicological properties (PCB congeners 138, 153, and 180), as previously suggested (Van Den Heuvel et al. 2002). We evaluated the associations between each organochlorine and NHL risk using linear splines: first with three boundaries (25th, 50th, and 75th percentiles) and then with nine boundaries placed at the 10th, 20th, 30th . . . 90th percentiles among all participants. The linearity was evaluated graphically in addition to being evaluated with a numerical test using the likelihood ratio test statistic to compare the model assuming lin- earity with the linear spline model. Because none of the organochlorines deviated from lin- earity (data not shown), we calculated IRR per interquartile range (IQR) based on the contin- uous organochlorine concentrations. The IRRs for NHL in association with concentrations of individual organochlorines in adipose tissue were calculated with and without adjusting for body mass index (BMI) as a continuous variable. Obesity has previously been associ- ated with NHL (Skibola 2007), and a high BMI could influence the adipose tissue con- centration of the organochlorine compounds. We estimated the linear effect of exposure for participants below and above the median BMI (26.0 kg/m2) among all participants and tested possible interactions by comparing these linear effect estimates. The potential sex-linked modification of the relationship between NHL risk and exposure to DDT, cis-nonachlor, and oxy- chlordane was also evaluated by introducing interaction terms into the model and testing by the Wald test. Finally, analyses were strati- fied by the time from adipose sampling to disease diagnosis for DDT, cis-nonachlor, and oxychlordane because stronger associations between NHL and organochlorine levels were previously reported in early (< median) com- pared with late (≥ median) follow-up periods in a study of three unrelated cohorts (Engel et al. 2007). Relationships between the different lipid- adjusted PCB congeners and pesticide analytes Environmental Health Perspectives • volume 120 | number 1 | January 2012 Non-Hodgkin lymphoma and organochlorine exposure detected over LOD were assessed among non- cases by the Spearman rank correlation. Results At baseline, cases were older (median, 64 years of age; range, 51–77 years) than subco- hort persons (median, 56 years of age; range, 50–65 years), 53% of cases and 46% of sub- cohort persons were obese (BMI ≥ 26), and sex distribution among cases (47% female) and subcohort persons (49% female) was similar. Organochlorines were quantified in most adipose tissue samples for p,p´-DDE, β-hexachlorocyclohexane, trans-nonachlor, hexachlorobenzene, and PCB congeners and in at least 56% of samples for the remaining organochlorines (Table 1). When controlling for age, sex, and BMI, we found suggestions of a monotonic dose– response relationship in association with con- centrations of DDT and cis-nonachlor, with respective IRRs for the highest versus lowest exposure categories of 1.64 (95% CI: 0.68, 3.96) and 2.52 (95% CI: 1.04, 6.09; Table 2). In the linear analyses, IRRs for IQR increases in exposure to DDT, cis-nonachlor and oxy- chlordane were 1.35 (95% CI: 1.10, 1.66), 1.13 (95% CI: 0.94, 1.36), and 1.11 (95% CI: 0.89, 1.38), respectively (Table 2). Estimates with and without adjusting for BMI (in addi- tion to controlling for sex and age) were simi- lar in both the linear and categorical analyses (Table 2). BMI did not significantly mod- ify the effect of any of the organochlorines, and p-values for the interaction were ≥ 0.16. Furthermore, the effects among obese per- sons (BMI ≥ 26) were not consistent for all the organochlorines, with enhanced effects observed for some and decreased effects for oth- ers (data not shown). We found no significant association or consistent trend between NHL risk and adipose concentrations of the five other pesticides or the chlordanes and DDT sums (Table 2), nor did we find any linear risk pattern for any of the individual PCB conge- ners or their sums (Table 3). We found higher relative risk estimates among men than women in association with DDT, cis-nonachlor, and oxychlordane (Table 4). The correlation between the organo- chlorine pesticides varied, with generally low correlations for dieldrin, hexachlorobenzene, and the other pesticides [rSpearman (rS) mostly < 0.30], strong correlations between the chlor- danes (rS = 0.74–0.91), and moderate correla- tion for the other pesticides (rS = 0.30–0.50). The PCBs were moderately to highly cor- related with each other [rS = 0.25–0.98; for a complete listing of correlation coefficients, see Supplemental Material, Table S2, (http:// dx.doi.org/10.1289/ehp.1103573)]. We found no significant difference in NHL risk among persons diagnosed in early follow-up (< 9.6 years after baseline) com- pared with those diagnosed in late follow-up [≥ 9.6 years after baseline; see Supplemental Material, Table S3 (http://dx.doi.org/10.1289/ ehp.1103573)]. Sensitivity analyses assign- ing persons with organochlorine levels below the LOD to the lowest exposure category (if the LOD for the actual sample was below the 25th percentile) or to a separate exposure cate- gory (for the remaining samples below the LOD) showed results similar to those from analyses excluding samples below the LOD (see Supplemental Material, Table S4). Discussion In this study, we found that lipid concentra- tions of DDT, cis-nonachlor, and oxychlor- dane in a general Danish population were associated with elevated risk of NHL. A posi- tive monotonic dose–response relationship was suggested for DDT and cis-nonachlor, Table 1. Organochlorines in adipose tissue from case and subcohort members. Above LOD [n (%)] Median (5th–95th percentile; μg/kg lipid) Compound p,p´-DDT p,p´-DDE β-Hexachlorocyclohexane cis-Nonachlor trans-Nonachlor Oxychlordane Dieldrin Hexachlorobenzene PCB-118 PCB-156 PCB-99 PCB-138 PCB-153 PCB-170 PCB-180 PCB-183 PCB-187 PCB-201 IQR (all; μg/kg lipid) 21 710 32 4.7 21 14 16 35 23 13 16.5 80 130 43 70 12 22 8 Cases 137 (57.3) 238 (99.6) 225 (94.1) 155 (64.9) 235 (98.3) 169 (70.7) 140 (58.6) 204 (85.4) 233 (97.5) 235 (98.3) 171 (71.5) 238 (99.6) 239 (100.0) 238 (99.6) 239 (100.0) 226 (94.6) 238 (99.6) 224 (93.7) Subcohort 137 (55.9) 237 (96.7) 220 (89.8) 156 (63.7) 232 (94.7) 171 (69.8) 144 (59.0) 213 (86.9) 233 (95.1) 236 (96.3) 177 (72.2) 243 (99.2) 244 (99.6) 243 (99.2) 245 (100.0) 227 (92.7) 240 (98.0) 227 (92.7) Cases 24 (9–83) 700 (180–2,400) 59 (31–110) 8.1 (3.5–17.0) 35 (17–76) 26 (15–47) 24 (9–49) 54 (20–120) 34 (16–70) 34 (20–61) 28 (14–57) 150 (57–270) 300 (170–470) 100 (65–170) 200 (120–340) 25 (11–40) 58 (29–92) 19 (11–33) Subcohort 21 (10–58) 640 (170–2,300) 56 (33–115) 6.8 (3.1–16.0) 32 (16–71) 23 (12–45) 18 (8–49) 52 (19–110) 35 (17–72) 34 (21–57) 26 (12–53) 140 (66–260) 300 (160–510) 100 (68–170) 200 (130–320) 24 (12–47) 56 (30–99) 19 (11–31) 107