Cotinine (Nicotine) ELISA Kit (DEIA6844)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
water, urine, saliva samples
Species Reactivity
N/A
Intended Use
The Cotinine ELISA is an immunoassay for the quantitative and sensitive detection of Cotinine. This test is suitable for the quantitative and/or qualitative screening of Cotinine in water, urine, and saliva samples. If necessary, positive samples can be confirmed by HPLC, GC/MS, or other conventional methods.
Contents of Kit
1. Microtiter plate
2. Standards (6)
3. Antibody Solution, 6 mL
4. Cotinine-HRP Conjugate Solution, 6 mL
5. Diluent/zero, 25 mL
6. Wash Solution (5X) Concentrate, 100 mL
7. Color Solution (TMB), 12 mL
8. Stop Solution, 12 mL
Storage
The Cotinine ELISA should be stored in the refrigerator (4-8°C). The solutions must be allowed to reach room temperature (20-25°C) before use. For more detailed information, please download the following document on our website.
Sensitivity
The estimated minimum detectable concentration, based on 90% B/Bo, is 0.045 ppb (μg/L) in water, 4.5 ppb (μg/L) in urine, and 9.0 ppb (μg/L) in saliva.

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References


Counseling alone or in combination with nicotine replacement therapy for treatment of black non-daily smokers: a randomized trial

ADDICTION

Authors: Nollen, Nicole L.; Cox, Lisa Sanderson; Mayo, Matthew S.; Ellerbeck, Edward F.; Ahluwalia, Jasjit S.

Background and aims One-third of US tobacco users are non-daily smokers (NDS). Black NDS have strikingly high levels of nicotine and carcinogen exposure. No smoking cessation studies have been conducted with this high-risk group. This study compared the effectiveness in black NDS of smoking cessation counseling alone or in combination with the participant's choice of nicotine replacement therapy. Design Two-arm parallel-group individually randomized clinical trial (allocation ratio of 2 : 1 intervention to control) Setting Academic medical and federally qualified health centers in three US cities. Participants Non-Hispanic black adult NDS receiving counseling with nicotine replacement therapy (C + NRT, n = 185) or counseling alone (C, n = 93). Interventions Twelve weeks of in-person and telephone smoking cessation counseling in combination with nicotine replacement therapy (NRT; C + NRT) or counseling alone (C). All participants received five sessions of counseling; those randomized to C + NRT received their choice of nicotine gum, patch and/or lozenge after a 9-day product trial period. The target quit day was set at 2 weeks post-baseline for both groups. Measurements Primary outcome was biochemically verified 30-day abstinence at week 12. Secondary outcomes were change in nicotine and carcinogen exposure [4-(methynitrosamino)-1-(3) pyridyle-1-butanol; NNAL] and tobacco consumption patterns. Findings Abstinence was 11.4% in C + NRT and 8.6% in C [odds ratio (OR) = 1.4, 95% confidence interval (CI) = 0.6, 3.2, P = 0.48]. Both groups experienced significant reduction in NNAL (C + NRT: 53% reduction, C: 50% reduction, within-group P < 0.0001) but non-significant changes in cotinine (P = 0.69). C + NRT reported more days abstinent (P < 0.001) and fewer total cigarettes (P = 0.002) compared with C. There was no evidence of compensation with other tobacco products. Conclusions Among black non-daily smokers in the United States, there was no difference in abstinence between nicotine replacement therapy (NRT) and counseling alone. NRT led to greater increase in days abstinent and reduction in cigarettes, with no evidence of compensation from other sources of nicotine.

Early life tobacco exposure and children's telomere length: The HELIX project

SCIENCE OF THE TOTAL ENVIRONMENT

Authors: Osorio-Yanez, Citlalli; Clemente, Diana B. P.; Maitre, Lea; Vives-Usano, Martha; Bustamante, Mariona; Martinez, David; Casas, Maribel; Alexander, Jan; Thomsen, Cathrine; Chatzi, Leda; Gutzkow, Kristine B.; Grazuleviciene, Regina; Martens, Dries S.; Plusquin, Michelle; Slama, Remy; McEachan, Rosemary C.; Wright, John; Yang, Tiffany C.; Urquiza, Jose; Tamayo, Ibon; Sunyer, Jordi; Vafeiadi, Marina; Nawrot, Tim S.; Vrijheid, Martine

Telomere length and mitochondrial DNA content are considered biomarkers of cellular aging, oxidative stress, and inflammation, but there is almost no information on their association with tobacco smoke exposure in fetal and early life. The aim of this study was to assess whether prenatal and childhood tobacco exposure were associated with leukocyte telomere length (LTL) and mitochondrial DNA (mtDNA) content in children. As part of a multi-centre European birth cohort study HELIX (Human Early-Life Exposome) (n = 1396) we assessed maternal smoking status during pregnancy through questionnaires, and through urinary cotinine levels that were then used to classify women as not exposed to smoking (<10 mu g/L), exposed to secondhand smoke (SHS) (10-50 mu g/L) and active smokers (>50 mu g/L). When the children were around 8 years of age (range: 5.4-12.0 years), childhood SHS tobacco smoke exposure was assessed through an extensive questionnaire and through measurements of urinary cotinine (<3.03 mu g/L non-detected, >3.03 mu g/L detected). Leukocyte mtDNA content and LTL were measured in the children at 8 years employing real time polymerase chain reaction (qPCR). Effect estimates were calculated using multivariate linear regression models for prenatal and childhood exposures adjusted for potential confounders. Maternal cotinine levels indicative of SHS exposure during pregnancy were associated with a decrease of 3.90% in LTL in children (95% CI: -6.68, -0.91), compared with nonsmoking, whereas the association for maternal cotinine levels indicative of active smoking did not reach statistical significance (-3.24%; 95% CI: -6.59, 0.21). Childhood SHS tobacco exposure was not associated with LTL in children. Global SHS exposure during childhood was associated with an increase of 3.51% (95% CI: 0.78, 6.27) in mtDNA content. Our findings suggest that tobacco smoke exposure during pregnancy, even at SHS levels, may accelerate telomere shortening in children and thus induce biological aging from an early age. (C) 2019 Elsevier B.V. All rights reserved.

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