Rainfall increases concentrations of Giardia and Cryptosporidium through its influence on turbidity, flow volume, and possibly other unidentified factors. An investigation of the variability of concentrations of Giardia cysts and Cryptosporidium oocysts in the Delaware River was conducted in 1996 at Trenton, N.J. A goal of the study was to examine the relationship between concentrations of Giardia and Cryptosporidium and a variety of more easily measured microbial, water quality, and meteorological parameters. A positive correlation (Spearman rank; p < 0.05) was demonstrated between concentrations of Giardia cysts or Cryptosporidium oocysts and 15 other parameters. Increased concentrations of Giardia and Cryptosporidium as well as a variety of other microorganisms were associated with rainfall. The effect of rainfall on parasite concentrations is due in part to increased particulate matter in the water column following surface runoff and resuspension of river bottom and storm drain sediment.

Following passage of the New Jersey Private Well Testing Act, 50,800 domestic wells were tested between 2002 and 2007 for the presence of total coliform (TC) bacteria. Wells containing TC bacteria were further tested for either fecal coliform or Escherichia coli (FC/E. coli) bacteria. Analysis of the data, generated by 39 laboratories, revealed that the rate of coliform detections in groundwater (GW) was influenced by the laboratory and the method used, and also by geology. Based on one sample per well, TC and FC/E. coli were detected in wells located in bedrock 3 and 3.7 times more frequently, respectively, than in wells located in the unconsolidated strata of the Coastal Plain. In bedrock, detection rates were higher in sedimentary rock than in igneous or metamorphic rock. Ice-age glaciers also influenced detection rates, most likely by removing material in some areas and depositing thick layers of unconsolidated material in other areas. In bedrock, coliform bacteria were detected more often in wells with a pH of 3 to 6 than in wells with a pH of 7 to 10 whereas the reverse was true in the Coastal Plain. TC and FC/E. coli bacteria were detected in 33 and 9.5%, respectively, of sedimentary rock wells with pH 3 to 6. Conversely, for Coastal Plain wells with pH 3 to 6, detection rates were 4.4% for TC and 0.6% for FC/E. coli.

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In compliance with the New Jersey Private Well Testing Act, 78,546 wells (93,787 samples, including samples from 13,290 wells that were analyzed more than once) were analyzed for total coliform (TC) bacteria by one or more of 39 laboratories over a 10‐year period. Samples containing TC bacteria were further analyzed for the presence of either fecal coliform or E. coli (FC/EC) bacteria. The large population of wells sampled multiple times permitted a systematic study of the effect of repeat sampling on coliform bacteria detection rates. The detection rate increased with the number of times wells were sampled. In bedrock, TC bacteria were detected in 21% of the population of wells analyzed only once, 33% in the population sampled twice, and 43% in the population sampled three times. It was estimated that TC bacteria would be detected in 90% of all wells if each well was analyzed 10 times. For FC/EC bacteria, it was estimated that 21 and 68 samples, respectively, would be required to reach the 50% and 90% population detection rates. In the Coastal Plain (CP), many more samples would be required to achieve the same estimated population detection rates. The population detection rate estimates were also dependent on the type of method used, the pH of the well water, and the geologic formation in which wells were located. A single sample was not sufficient to detect coliform bacteria when present in well water.

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Detecting fecal waste contamination of groundwater is usually accomplished by testing for fecal “index” or “indicator” bacteria. The authors examined 128 samples from 26 public groundwater sources in New Jersey and compared the ability of nine potential indicators to detect fecal contamination. Each sample was tested for heterotrophic plate count; total coliform (TC); fecal coliform (FC); Escherichia coli, enterococci, and Clostridium perfringens bacteria (100 mL); somatic and F+ coliphage (100 mL); and coprostanol (1 and 4 L). Data from a source with known contamination showed that the TC test was the most reliable indicator, followed by the FC test. Fecal pollution contains high concentrations of TC bacteria, but because some TC bacteria in the environment may not be of fecal origin, a positive TC test result should be followed by an FC, E. coli, or enterococci test to confirm contamination. The sanitary significance of the occasional presence of TC bacteria or coliphage without other fecal indicators was uncertain. Methods capable of analyzing 1‐L volumes should be investigated. A groundwater should be analyzed multiple times (i.e., 10 or more) to confidently determine its sanitary status.

It is important that indicators of fecal pollution are reliable. Coliform bacteria are a commonly used indicator of fecal pollution. As other investigators have reported elsewhere, we observed a seasonal pattern of coliform bacteria detections in domestic wells in New Jersey. Examination of a statewide database of 10 years of water quality data from 93,447 samples, from 78,207 wells, generated during real estate transactions, revealed that coliform bacteria were detected in a higher proportion of wells during warm weather months. Further examination of the seasonal pattern of other data, including well water pH, precipitation, ground and surface water temperatures, surface water coliform bacteria concentrations, and vegetation, resulted in the hypothesis that these bacteria may be derived from nonfecal (or environmentally adapted) as well as fecal sources. We provide evidence that the coliform seasonality may be the result of seasonal changes in groundwater extraction volumes (and to a lesser extent precipitation), and temperature‐driven changes in the concentration of surface or near‐surface coliform sources. Nonfecal coliform sources may not indicate the presence of fecal wastes and hence the potential presence of pathogens, or do so in an inconsistent fashion. Additional research is needed to identify the sources of the coliforms detected in groundwater.

Metabolic activation of benzo[a]pyrene (BaP) by cellular enzymes is required for DNA adduct formation. In vivo DNA adducts might also arise from BaP metabolites supplied via the systemic circulation, rather than from in situ activation. We determined whether electrophilic metabolites could be detected in mouse serum 4 h after BaP dosing (i.p.) by trapping metabolites with salmon sperm DNA (ssDNA), followed by 32P-postlabeling analysis for DNA adducts. In vitro studies demonstrated that mouse serum sequesters BaP-7,8-diol-9,10-epoxide (BPDE) and protects it from hydrolysis. BPDE was rapidly transferred from serum to ssDNA or splenocytes, with adduct levels in ssDNA 4- to 7-fold greater than in splenocytes. After BaP administration, mouse serum produced two adduct spots when incubated with ssDNA. The major adduct (spot 3) co-chromatographed with a BPDE adduct standard, while the minor adduct (spot 2) was unrelated to BPDE. A BPDE standard curve in control serum was developed to quantitate BPDE levels in dosed serum. These levels ranged from 13.1 to 19.1 nM. Tissue DNA contained three adduct spots: spots 2 and 3 appeared identical to the respective adducts arising from dosed serum. BPDE-DNA adducts in tissues were highest in liver, lung and spleen, with kidney and stomach levels significantly lower. Levels of adduct 2 did not correlate with levels of adduct 3, especially in spleen where the adduct 2/adduct 3 ratio was very low. In vitro studies in which splenocytes were presented with both adducting metabolites suggested that splenocytes preferentially form adduct 3. These results indicate that two of the three BaP electrophilic metabolites responsible for cellular DNA damage are present in mouse serum. The levels of BPDE in serum may be sufficient to account for a substantial portion of the tissue load of BPDE-DNA adducts.