Material for Containers
Sarfaraz K. Niazi in Handbook of Pharmaceutical Manufacturing Formulations, Third Edition, 2019
Materials based on nonplasticized poly(vinyl chloride) that comply with the following specifications are suitable for the manufacture of containers for noninjectable aqueous solutions. Plastic containers for aqueous solutions for infusion are manufactured from one or more polymers, if necessary with additives. A plastic container for pharmaceutical use is a plastic article that contains or is intended to contain a pharmaceutical product and is, or may be, in direct contact with it. The closure is a part of the container. Rubber closures for containers for aqueous parenteral preparations for powders and for freeze-dried powders are made of materials obtained by vulcanization of macromolecular organic substances with appropriate additives. The specification also applies to closures for containers for powders and freeze-dried products to be dissolved in water immediately before use. The manufacturer of the product must ensure that containers made in production are similar in every respect to the type samples.
Examples from the Chemical Industry
John Andraos in Synthesis Green Metrics, 2018
This chapter presents 40 culminating problems covering all of the ladder concepts. These are applied to determining the material efficiency, environmental impact, safety-hazard impact, and energy efficiency of synthesis plans to various pharmaceuticals and industrially important commodity chemicals. The problems cover the following kinds of techniques: preparation of solutions, batch processes, microchannel technology, biofeedstocks, continuous flow microwave, scale-up versus scale-out, and synthesis plan analysis Biopolymers made from itaconic acid are possible substitutes for petrochemical based polymers made from acrylic acid or methacrylic acid. Vinyl chloride is a high volume industrial chemical that is primarily used to make polyvinyl chloride. Process water mass intensity is the mass difference between freshwater usage and recycled water usage per unit mass of product made. Sodium anthraquinone-2-sulfonate, which is called “silver salt” in the industry because of its appearance, can be recrystallized from water to produce a material which is almost chemically pure.
Hydrocarbons
Thomas A. Gossel, J. Douglas Bricker in Principles of Clinical Toxicology, 2018
Hydrocarbons comprise a broad group of organic compounds that contain only hydrogen and carbon. They may be divided into two large categories: aliphatic (straight chain) or aromatic (benzene ring) compounds. Another group, which is of great toxicologic significance, consists of halogenated aliphatic and arpmatic hydrocarbons. Some of these are discussed in this chapter; others, such as organochlorine insecticides, are described in other chapters. Hydrocarbons commonly encountered in acute poisonings consist of a mixture of saturated and unsaturated, aliphatic, ali-cyclic, or aromatic compounds and are usually distillates of crude oil, coal tar, and pine wood. Examples of each of these groups are presented in Table 7.1 . Table 7.1 Hydrocarbon classification Aliphatic Gases — methane, propane, butane Liquids — hexane, octane, etc. Waxes — paraffins Aromatfcs Benzene, toluene, xylene, styrene, vinyl chloride Halogenated Aliphatic — chloroform, carbon tetrachloride methylene chloride Aromatic — DOT, a chlordane, lindane, p -dichtorobenzene, polychlorinated biphenyls Petroleum distillates Petroleum ether (benzine), gasoline, naphtha kerosene, fuel oil, lubricating oil, paraffin, asphalt Distillates of pine wood Turpentine Distillates of coal tar Benzene, cumene, toluene, xylene a DDT, dichlorodlphenyltrichloroethane.
A novel potentiometric biosensor for determination of L-lysine in commercial pharmaceutical L-lysine tablet and capsule
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2016
The construction of an L-lysine biosensor on ammonium-selective poly(vinylchloride) (PVC) membrane electrode is described in this study. The construction procedure occurs in two stages: (I) the preparation of ammonium-selective poly(vinylchloride) (PVC) membrane electrode and (II) the chemical immobilization of lysine oxidase on this ammonium-selective electrode by using glutaraldehyde. The ammonium ions produced after enzymatic reaction were determined potentiometrically. The sensitivity of the lysine biosensor against ammonium ions and lysine were studied. The response time, linear working range, reproducibility and life time of the biosensor were also determined. The interfering effect of other amino acids on the biosensor performance was also studied and potentiometric selectivity coefficients were calculated. Although the biosensor responded mainly against tyrosine, a lot of amino acids and ascorbic acid that can be present in some real samples did not show any important interference. Additionally, lysine assay in commercial pharmaceutical lysine tablets and capsules was also successfully carried out. The results were in good agreement with previously reported values.
Gene–environment interactions between DNA repair polymorphisms and exposure to the carcinogen vinyl chloride
Published in Biomarkers, 2009
Yongliang Li, Marie-Jeanne Marion, Jennifer Zipprich, Regina M. Santella, Greg Freyer, Paul W. Brandt-Rauf
We have recently suggested that polymorphisms in metabolism and repair pathways may play a role in modulating the effects of exposure to the carcinogen vinyl chloride in the production of biomarkers of its mutagenic damage. The aim of the present study was to extend these observations by examining gene–environment interactions between several common polymorphisms in the DNA repair genes XRCC1 and ERCC2/XPD and vinyl chloride exposure on the production of vinyl chloride-induced biomarkers of mutation. A cohort of 546 French vinyl chloride workers were genotyped for the XRCC1 codon 194 (Arg>Trp; rs1799782), 280 (Arg>His; rs25489) and 399 (Arg>Gln; rs25487) polymorphisms and the ERCC2/XPD codon 312 (Asp>Asn; rs1799793) and 751 (Lys>Gln; rs13181) polymorphisms. The results demonstrated a statistically significant allele dosage effect of the XRCC1 399 variant on the production of the vinyl chloride-induced mutant p53 biomarker, even after controlling for confounders including cumulative vinyl chloride exposure (p = 0.03), with a potentially supramultiplicative gene–environment interaction. In addition, the results demonstrate statistically significant allele dosage effects of the ERCC2/XPD 312 and 751 variants on the production of the vinyl chloride-induced mutant ras-p21 biomarker, even after controlling for confounders including cumulative vinyl chloride exposure (p < 0.0001 and p = 0.0006, respectively), with a potentially supramultiplicative gene–environment interaction for the codon 751 allele. Finally, the results suggest potential supramultiplicative gene–gene interactions between CYP2E1 (c2 allele; rs3813867) and ERCC2/XPD polymorphisms that are consistent with the proposed carcinogenic pathway for vinyl chloride, which requires metabolic activation by CYP2E1 to reactive intermediates that form DNA adducts that, if not removed by DNA repair mechanisms, result in oncogenic mutations.
Vinyl Chloride—A Classical Industrial Toxicant of New Interest
Published in Critical Reviews in Toxicology, 2005
The carcinogenicity of vinyl chloride in humans was recognized in 1974 based on observations of hepatic angiosarcomas in highly exposed workers. A multiplicity of endpoints has been demonstrated. The primary target organ, the liver, displays differential susceptibilities of hepatocytes and sinusoidal cells, which are modified by factors of age and dose. There is consistency in organotropism between experimental animals and humans. Vinyl chloride is a pluripotent carcinogen, predominantly directed toward hepatic endothelial (sinusoidal) cells, and second toward the parenchymal cells of the liver. The similarity of results between experimental animals and humans is a solid basis of an amalgamation of experimental and epidemiological risk estimates. Vinyl chloride requires metabolic activation for carcinogenicity and mutagenicity, and toxicokinetics are a key to interpret the dose response. Practically the entire initial metabolism of vinyl chloride is oxidative. At higher exposure concentrations this is nonlinear, and metabolic saturation of metabolism in rats is reached at about 250 ppm. This is consistent with the plateau of hepatic angiosarcoma incidence in rat bioassays. Physiologically based pharmacokinetic/toxicokinetic (PBPK) models have been developed and successfully applied within the frame of human cancer risk assessments. The major DNA adduct induced by vinyl chloride (∼ 98% of total adducts in rats), 7-(2-oxoethyl)guanine, is almost devoid of promutagenic activity. The clearly promutagenic “etheno” adducts N2,3-ethenoguanine and 3,N4-ethenocytosine each represent ∼ 1% of the vinyl chloride DNA adducts in rats, and 1,N6-ethenoadenine is found at even lower concentrations. Etheno adducts appear to have a long persistence and are repaired by glycosylases. Vinyl chloride represents a human carcinogen for which a series of mechanistic events connects exposure with the carcinogenic outcome. These include (1) metabolic activation (to form chloroethylene oxide), (2) DNA binding of the reactive metabolite (to exocyclic etheno adducts), (3) promutagenicity of these adducts, and (4) effects of such mutations on protooncogenes/tumor suppressor genes at the gene and gene product levels. In rat hepatocytes, a further event is a biomarker response. Cancer prestages (enzyme-altered foci), as quantitative biomarkers, provide a tool to study dose response even within low dose ranges where a carcinogenic risk cannot be seen in cancer bioassays directly. Such biomarker responses support a linear nonthreshold extrapolation for low-dose assessment of carcinogenic risks due to vinyl chloride. Published risk estimates based on different sets of data (animal experiments, epidemiological studies) appear basically consistent, and on this basis an angiosarcoma risk of ∼ 3 × 10−4 has been deduced by extrapolation, for exposure to 1 ppm vinyl chloride over an entire human working lifetime. An important point that should be considered in regulatory standard settings is the presence of a physiological background of those etheno DNA adducts, which are also produced by vinyl chloride. Likely reasons for this background are oxidative stress and lipid peroxidation. In essence, fundamentals of the hepatocarcinogenicity of vinyl chloride appear now well established, providing a solid scientific basis for regulatory activities.
Related Knowledge Centers
- Ethanol
- Ethylene
- Vinyl Compounds
- Ch
- Chlorinated Hydrocarbons
- Chlorine
- Volatile Anesthetic