Susan A. Korrick

Dr. Susan A. Korrick

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Research Focus & Metrics

Academic Career Length

29Years (1998-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 December 2014 in Clinical Immunology
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Journal Article
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Kari NadeauKari Nadeau
Kari Nadeau
ZLZhigang Li
Zhigang Li
SFShohreh Farzan
Shohreh Farzan
DKDevin C Koestler
Devin C Koestler
DRDavid J. Robbins
David J. Robbins
MKMargaret R. Karagas
Margaret R. Karagas

1 March 1999 in American Journal of Public Health
Verified
Journal Article
Closed access
SKSusan A. Korrick
Susan A. Korrick
DHD J Hunter
D J Hunter
ARA Rotnitzky
A Rotnitzky
HHH Hu
H Hu
FSF E Speizer
F E Speizer
The role of lead exposure as a risk factor for hypertension is less well defined among women than among men. This case-control study assessed the relation of blood and bone lead concentrations to hypertension in women. Cases and controls were a subsample of women from the Nurses' Health Study. Hypertension was defined as a physician diagnosis of hypertension between 1988 and 1994 or measured systolic blood pressure > or = 140 mm Hg or diastolic blood pressure > or = 90 mm Hg. Mean (SD) blood lead concentration was 0.15 (0.11) mumol/L; mean tibia and patella lead concentrations by K-x-ray fluorescence were 13.3 (9.0) and 17.3 (11.1) micrograms/g, respectively. After adjustment for potentially confounding factors, an increase from the 10th to the 90th percentile of patella lead values (25 micrograms/g) was associated with approximately 2-fold (95% confidence interval = 1.1, 3.2) increased risk of hypertension. There was no association between hypertension and either blood or tibia lead concentrations. These findings support a potentially important role for low-level lead exposure as a risk factor for hypertension among non-occupationally exposed women.

1 April 2008 in Current Opinion in Pediatrics
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Journal Article
Closed access
SKSusan A. Korrick
Susan A. Korrick
SSSharon K Sagiv
Sharon K Sagiv
Purpose of review Although environmental levels of polychlorinated biphenyls and certain organochlorine pesticides – hexachlorobenzene, dichlorodiphenyl trichloroethane and its primary metabolite, dichlorodiphenyl dichloroethene – are generally on the decline, early-life exposures to these prevalent contaminants continue. The review will describe current understanding of the potential neurodevelopmental consequences of low-level exposures to these contaminants. Recent findings Animal models suggest that early-life exposures to polychlorinated biphenyls, dichlorodiphenyl trichloroethane/dichlorodiphenyl dichloroethene or hexachlorobenzene are associated with decreased cognitive or behavioral function in later development. Despite almost 30 years of research, however, results of human studies are inconsistent regarding the nature of the observed effects and their persistence over time. Overall, epidemiologic studies support modest associations of primarily prenatal polychlorinated biphenyl exposures with differences in neuromotor development, decrements in cognition and behavioral deficits, particularly regarding attention and impulse control. There are limited published human data regarding potential neurodevelopmental toxicities of early-life exposures to dichlorodiphenyl trichloroethane/dichlorodiphenyl dichloroethene and hexachlorobenzene. Summary Exposures to polychlorinated biphenyls, dichlorodiphenyl trichloroethane/dichlorodiphenyl dichloroethene and hexachlorobenzene are likely detrimental to neurodevelopment. Effective control of exposure is complicated by variable exposure sources and variable contaminant levels in food, particularly fish, for which it is important to balance the risk of contaminants with nutritional benefits.

1 November 2000 in Journal of Exposure Science & Environmental Epidemiology
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Journal Article
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SKSusan A. Korrick
Susan A. Korrick
LALarisa M Altshul
Larisa M Altshul
PTPaige E Tolbert
Paige E Tolbert
VBVirlyn W Burse
Virlyn W Burse
LNLarry L Needham
Larry L Needham
RMRichard R Monson
Richard R Monson

1 May 2010 in Pediatrics
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Journal Article
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PWPaige Williams
Paige Williams
OSOleg Sergeyev
Oleg Sergeyev
MLMary M. Lee
Mary M. Lee
SKSusan A. Korrick
Susan A. Korrick
JBJane S. Burns
Jane S. Burns
RHRuss Hauser
Russ Hauser
OBJECTIVE: We evaluated the association of blood lead levels (BLLs) with pubertal onset in a longitudinal cohort of Russian boys. METHODS: A total of 489 Russian boys were enrolled in 2003–2005, at 8 to 9 years of age, and were monitored annually through May 2008. Cox proportional-hazards models were used to evaluate the association of BLLs at enrollment with time to pubertal onset during follow-up monitoring. RESULTS: A total of 481 boys had BLLs, with a median of 3 μg/dL and 28% with values of ≥5 μg/dL. The proportion of pubertal boys increased with age, from 12% at age 8 to 83% at age 12 for testicular volume of >3 mL, from 22% to 90% for genitalia stage 2 or higher, and from 4% to 40% for pubic hair stage 2 or higher. After adjustment for potential confounders including BMI and height, boys with high BLLs (≥5 μg/dL) had 24% to 31% reduced risk of pubertal onset, on the basis of testicular volume of >3 mL (hazard ratio [HR]: 0.73 [95% confidence interval [CI]: 0.55–0.97]; P = .03), genitalia staging (HR: 0.76 [95% CI: 0.59–0.98]; P = .04), and pubic hair staging (HR: 0.69 [95% CI: 0.44–1.07]; P = .10), compared with those with lower BLLs. Pubertal onset occurred 6 to 8 months later, on average, for boys with high BLLs, compared with those with BLLs of <5 μg/dL. CONCLUSION: Higher BLLs were associated with later pubertal onset in this prospective study of peripubertal Russian boys.

15 August 2002 in American Journal of Epidemiology
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Journal Article
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SKSusan A. Korrick
Susan A. Korrick
JSJoel Schwartz
Joel Schwartz
STShirng-Wern Tsaih
Shirng-Wern Tsaih
DHDavid J. Hunter
David J. Hunter
AAAntonio Aro
Antonio Aro
HHHoward Hu
Howard Hu
In 1993–1995, the authors evaluated risk factors for elevated blood and bone lead levels in 264 Boston, Massachusetts, area women previously selected for a case-control study of lead and hypertension. Bone lead was measured at the tibia and patella with K x-ray fluorescence. Blood lead was analyzed by graphite furnace atomic absorption. Participants were aged 46–74 years and had mean lead levels of 3 (standard deviation, 2) µg/dl (blood), 13 (standard deviation, 9) µg/g (tibia), and 17 (standard deviation, 11) µg/g (patella). In multivariate linear regression models, use of postmenopausal estrogen (inverse) and alcohol intake (positive) were significantly associated with blood lead levels. Both bone lead measures were significantly and positively associated with blood lead but only among postmenopausal women not using estrogen; for example, an increase from the first to the fifth quintile of tibia lead level (19 µg/g) was associated with a 1.7-µg/dl increase in blood lead (p = 0.0001) in this group. Older age and lower parity were associated with higher tibia lead; only age was associated with patella lead. The observed interaction of bone lead with estrogen status in determining blood lead supports the hypothesis that increased bone resorption, as occurs postmenopausally because of decreased estrogen production, results in heightened release of bone lead stores into blood.